(Circulation. 1999;99:348-353.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Shed Membrane Microparticles With Procoagulant Potential in Human Atherosclerotic Plaques
A Role for Apoptosis in Plaque Thrombogenicity
From the Institut National de la Santé et la Recherche Médicale, INSERM U141, IFR "Circulation," Hôpital Lariboisière, Paris, France (Z.M., A.T.); Institut d'Hématologie et d'Immunologie, Faculté de Médecine, Université Louis Pasteur, Strasbourg, France and INSERM U143, Le Kremlin-Bicêtne, France (B.H., J.-M.F.); and Service de Chirurgie Thoracique et Vasculaire, Hôpital Beaujon, Clichy, France (J.O., G.L.).
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Abstract |
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Background—The specific role of apoptosis in human atherosclerosis remains unknown. During apoptotic cell death, phosphatidylserine exposure on the cell surface confers a high tissue-factor (TF)–dependent procoagulant activity.
Methods and Results—In this study, we examined the role of apoptotic cell death in the promotion of plaque thrombogenicity. TF expression and its relation to apoptosis was analyzed in 16 human atherosclerotic plaques by the use of immunohistochemical techniques. The presence of shed membrane apoptotic microparticles was analyzed in extracts from 6 human atherosclerotic plaques and 3 underlying arterial walls. The microparticles were captured by annexin V and their amounts estimated with respect to their phospholipid content by use of a prothrombinase assay. The prothrombogenic potential of the microparticles was further assessed by the measurement of total and microparticle-dependent TF activity in the extracts. The cell origin of the microparticles was determined after capture by specific antibodies. We were able to detect marked TF expression in the plaques in close proximity to apoptotic cells and debris, suggesting a potential interaction between TF and the apoptotic cell surfaces. High levels of shed membrane apoptotic microparticles were detected in extracts from atherosclerotic plaques but not in the underlying arterial walls (29.5±3.7 nmol/L phosphatidylserine equivalent versus 1.3±0.4 nmol/L, respectively, P<0.02). The microparticles were mainly of monocytic and lymphocytic origin and retained 97±2% of total TF activity, indicating a direct causal relationship between shed membrane microparticles and procoagulant activity of plaque extracts.
Conclusions—These results indicate that shed membrane microparticles with procoagulant potential are produced in human atherosclerotic plaques. Apoptosis could be a critical determinant of plaque thrombogenicity after plaque rupture.
Key Words: apoptosis • thrombosis • atherosclerosis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Apoptosis is a process of cell death that occurs during the development and progression of human atherosclerotic plaques.1 2 3 4 5 6 7 Much interest has focused on the regulation of apoptosis in atherosclerosis and plaque-derived cells,1 3 6 7 8 but only speculations have been raised about the potential role, beneficial or harmful, of this local process of cell death in atherosclerosis. Death of macrophages and T lymphocytes by apoptosis, a process with no or limited inflammatory response, might be viewed as beneficial. On the other hand, apoptotic death of smooth muscle cells, which may weaken the fibrous cap and contribute to plaque rupture, can be considered as harmful. However, there is no direct evidence to support these speculations. Recent studies have shown that apoptotic cells and microparticles exhibit marked procoagulant activity.9 10 11 12 13 14 This consequence of apoptosis is potentially deleterious in atherosclerosis because it might enhance plaque thrombogenicity after plaque rupture and lead to acute ischemic events and infarction.
Defined components of human atherosclerotic plaques are highly thrombogenic15 16 and express high levels of tissue factor (TF).16 17 18 19 20 Active TF is also present in atherosclerotic plaques.21 22 However, the exact mechanism(s) responsible for the enhanced TF activity and the enhanced prothrombogenic properties of certain plaque components are still poorly understood. TF activity is operational on the surface of cell membranes and it is highly dependent on the presence of anionic phospholipids, chiefly phosphatidylserine.23 24 25 26 27 Interestingly, phosphatidylserine is redistributed to the external membrane layer during apoptotic cell death28 and confers a procoagulant activity to the apoptotic cell surface.9 10 Recently, we have shown11 29 that shed membrane microparticles arising from cell fragmentation during apoptosis also retain procoagulant properties. However, it is not known whether shed membrane microparticles are produced in atherosclerotic plaques or whether they are implicated in the local activation of TF. This study was undertaken to examine (1) TF expression in apoptotic regions of human atherosclerotic plaques, (2) the presence of shed membrane microparticles in human atherosclerotic plaques, and (3) the procoagulant potential of these microparticles. In this study, we provide direct evidence that shed membrane apoptotic microparticles are produced in human atherosclerotic plaques and retain membrane-associated procoagulant activities. Apoptosis may therefore play a major role in the amplification of acute thrombotic events after plaque rupture.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Materials
Twenty-two human atherosclerotic plaques, removed from 20 patients undergoing carotid endarterectomy and 2 patients undergoing resection of abdominal aortic aneurysm, were collected. Sixteen plaques were processed for immunohistochemical studies. A piece from the most stenotic area of each arterial specimen was immediately placed for 2 hours in fresh 4% paraformaldehyde, then transferred to a 30% sucrose-PBS solution before being embedded in paraffin. Other adjacent segments of the stenotic area were snap frozen in optimal cutting temperature tissue processing medium (O.C.T. Compound, Miles Inc, Diagnostics Division) with liquid nitrogen and stored at -80°C for cryostat sectioning. For each specimen, several 5- to 6-µm sections were obtained for histological analysis, in situ detection of apoptosis, and immunohistochemical studies.
Six freshly removed advanced (complicated) human atherosclerotic plaques and 3 underlying, macroscopically normal, arterial walls were used for extraction of apoptotic microparticles.
In Situ Detection of Apoptotic Cell Death
In situ detection of apoptotic cells was performed on
cryostat sections by the use of terminal
deoxynucleotidyltransferase-mediated
dUTP nick-end labeling of fragmented DNA (TUNEL method), as previously
described.6 To enhance the specificity of the staining,
prefixation time was abrogated and treatment of sections with
proteinase k was omitted.30
Immunohistochemistry
Cryostat sections were incubated with 1:10 normal horse serum
for 30 minutes at room temperature, washed once in PBS, then incubated
with a primary mouse monoclonal antibody against TF (anti-human TF,
type 2, Calbiochem) at a dilution of 5 µg/mL. After they were washed
in PBS, the slides were incubated with a secondary biotinylated horse
anti-mouse IgG (Vector Laboratories, Inc) at a dilution of 1:200.
Immunostains were visualized with the use of avidin-biotin
horseradish peroxidase (brown staining) or alkaline phosphatase (red
color) visualization systems (Vectastain ABC Kit, standard and elite,
Vector Red, Vector Laboratories). For negative controls, adjacent
sections were stained with mouse IgG instead of the primary antibody.
For double staining with TUNEL, sections were first stained with the
specific anti-TF antibody as described above before they were processed
for in situ detection of apoptosis by use of TUNEL.
Extraction of Apoptotic Microparticles From Arterial
Tissue
Six freshly removed complicated atherosclerotic plaques were
abundantly rinsed in different cold HBSS solutions supplemented with
glucose, amino acids, and antibiotics (100 IU/mL penicillin and 100
µg/mL streptomycin). Under a sterile hood and on ice, the
atherosclerotic plaque was rapidly separated from the underlying
arterial wall and minced (200 mg of tissue from each
plaque). The microparticles were released from the minced plaque by use
of a previously described enzymatic digestion procedure for extraction
of plaque-derived cells.31 The released cells were
pelleted at 500g and the supernatant centrifuged at
12 000g for 1 minute.29 The remaining
supernatant containing the microparticles was stored at -80°C for
further analysis. The underlying, and macroscopically normal,
arterial wall (200 mg of tissue) from 3 of these plaques
was processed in an identical manner and served as control.
Detection of Apoptotic Microparticles
Microparticles were captured by immobilized annexin
V as previously described.29 In brief, annexin V was
biotinylated (annexin VBi) and then insolubilized
onto streptavidin-coated microtitration plates. After incubation for 30
minutes at room temperature, the plates were washed 3 times with
TBS-Ca2+. Plaque or underlying
arterial wall supernatant was then added and remained
in contact with insolubilized annexin VBi
for 30 minutes at room temperature in the presence of 10 mmol/L
Ca2+ added to HBSS. After the plates were washed,
their anionic phospholipid content was determined by prothrombinase
assay. In the assay, the blood clotting factor and calcium
concentrations (factor Xa, factor V(a), prothrombin, and
CaCl2) were determined to ensure that
phosphatidylserine is the rate-limiting
parameter of the reaction.29 After a 2-hour
incubation at 37°C, the reaction was stopped by addition of 5
mmol/L EDTA. After addition of Chromozym TH, a chromogenic
substrate for thrombin, linear absorbance changes were recorded at
405 nm by the use of a microtitration plate reader equipped with
kinetics software. Results were expressed as nanomolar
phosphatidylserine equivalent by reference to a
standard curve constructed by the use of liposomes of defined
composition.29
Antigenic Capture and Characterization of Released
Particles
Biotinylated antibodies (anti-CD11a, anti-CD4, and anti-GP Ib)
were insolubilized onto streptavidin-coated microtitration plates.
After incubation for 30 minutes at room temperature, the plates were
washed 3 times with TBS-Ca2+. Plaque or
underlying arterial wall supernatant was then added and
incubated for 2 hours at room temperature before the plates were
again washed 3 times with TBS-Ca2+.
Microparticle detection was achieved by prothrombinase assay as
described above. Background values obtained with irrelevant IgGs were
subtracted from those measured with specific monoclonal antibodies
(mAbs).
Determination of Total and Microparticle-dependent TF
Activity
TF was measured in the whole supernatants before and after
removing shed membrane microparticles by
ultracentrifugation at 400 000g, 90
minutes, 20°C.32 TF activity was determined through
its ability to promote the activation of factor X by factor VII(a) in
the presence of CaCl2, exactly as described by
Satta et al.14 The reaction proceeded for 30 minutes at
37°C and was stopped by addition of an excess of EDTA.
Chromogenic substrate for factor Xa, S-2765, was added and
the change in absorbance at 405 nm versus time was immediately
recorded by the use of a microtitration plate reader equipped with
kinetics software. Results were expressed as nanomolar of factor Xa
generated in the assay by reference to a standard curve constructed
with known amounts of factor Xa.
In control experiments, inhibition of TF was fully achieved by a specific mAb added at a final concentrations of 1 µg/mL and 6 µg/mL just before factors VII and X.
Statistical Analysis
Results are expressed as mean±SEM. Comparisons between groups
were made by use of the Mann-Whitney U test.
P<0.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Association of TF and Apoptosis in Human Atherosclerotic Plaques
We first examined the relation between TF expression and apoptosis in 16 human carotid and abdominal aortic atherosclerotic plaques. We consistently detected high levels of TF expression in acellular regions of plaques. Analyzing serial adjacent sections and double-stained sections, we found that these acellular areas were also strongly positive for TUNEL (Figure
A), suggesting that they are the result
of extensive apoptotic cell death. Positive staining for TUNEL
in these acellular areas suggests that they might be rich in shed
membrane apoptotic microparticles stemming from
apoptotic cells. Therefore, TF may be present in close
contact with phosphatidylserine in these areas, a
condition that would considerably enhance its
activity.23 24 25
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Apoptosis also occurs in cellular regions of atherosclerotic
plaques.2 3 4 5 6 7 Analysis of serial adjacent sections
and double-stained sections showed that there is significant TF
expression in these apoptotic regions (Figure
B and C).
Interestingly, significant extracellular staining for TF was observed
in these areas (Figure B and C), suggesting that TF is released
from the cell, possibly in apoptotic microparticles, during
cell death. No staining was observed in sections probed with irrelevant
IgG (Figure D).
Presence of Shed Membrane Microparticles With Procoagulant
Potential in Atherosclerotic Plaques
On the basis of these results, we hypothesized that shed membrane
microparticles bearing phosphatidylserine may be
produced in the plaque, and that these microparticles may retain
significant TF activity and therefore be highly thrombogenic. To
examine the presence of microparticles in human atherosclerotic tissue,
6 fresh atherosclerotic plaques were obtained after carotid
endarterectomy and were enzymatically digested by
use of an already described procedure for isolation of plaque-derived
cells.31 Underlying arterial walls of 3 of
these plaques served as controls. Levels of shed membrane
microparticles were then determined with respect to their procoagulant
phospholipid content by a prothrombinase assay. We detected high levels
of phosphatidylserine-bearing microparticles in the
6 atherosclerotic plaques but very low levels in the 3 underlying
arterial walls (29.5±3.7 nmol/L
phosphatidylserine equivalent [23.2 to 45.9
nmol/L] versus 1.3±0.4 nmol/L [0.6 to 1.8 nmol/L], respectively,
P<0.02) (Table).
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To further evaluate the prothrombogenic properties of the shed membrane microparticles, we determined TF activity in supernatants before and after the removal of the microparticles by ultracentrifugation. We found that total TF activity was significantly elevated in the extracts of plaques in comparison with those of underlying arterial walls (8.3±4.3 nmol/L of generated factor Xa [2.8 to 25.6 nmol/L] versus 0.9±0.1 nmol/L [0.7 to 1.1 nmol/L], respectively, P<0.03) (Table). Interestingly, the removal of microparticles from plaque supernatants by ultracentrifugation resulted in 97±2% loss of TF activity, indicating that almost all TF activity of plaque extracts was associated with shed membrane microparticles.
Cell Origin of Shed Membrane Microparticles
To identify particle-associated antigens, extracts of
plaques were incubated with corresponding insolubilized mAbs. Smooth
muscle cells, macrophages, and T lymphocytes are the 3 major
cell types present in the plaque. Rare mast cells are also
encountered. However, we6 and others5 have
shown that macrophages and lymphocytes form the bulk of
apoptotic cells in the plaque. Therefore, in an attempt to
characterize the cell origin of the particles, anti-CD11a, anti-CD4,
and anti-GP Ib mAbs were used. There were no particles bearing GP Ib in
the extracts. Most particles recovered from plaques were of monocytic
and lymphocytic origin (19.2±13.4 nmol/L
phosphatidylserine equivalent and 10.9±2.8 nmol/L
phosphatidylserine equivalent after capture by
anti-CD11a or anti-CD4, respectively), a finding that reflects the cell
types undergoing apoptosis in the plaque. No direct comparison
between capture by annexin V and mAbs could be done because of
different preincubation times and affinities for the respective
ligands.29 However, these experiments establish that
particles from supernatants of plaques bear a proportion of antigens
found on the corresponding cell surfaces.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Apoptosis is a common event that occurs in atherosclerosis.1 2 3 4 5 6 7 However, no direct evidence has been provided for a beneficial or a harmful role for this process in plaque development and progression. In this study, we examined the role of in situ apoptotic cell death in the promotion of plaque thrombogenicity.
TF is a key element in the initiation of the coagulation cascade. In the normal vessel, TF expression is restricted to the adventitia17 and contributes to vessel repair after vessel injury. Enhanced TF expression and activity have been reported in human atherosclerotic plaques,16 17 18 19 20 21 22 and it is now believed that the increase of TF activity is a major determinant of plaque thrombogenicity. However, TF activity is highly dependent on the presence of phosphatidylserine,24 25 26 27 and it has recently been shown that apoptotic cell death results in phosphatidylserine exposure on the cell surface conferring a potent procoagulant activity to the cell.9 10 11 12 13 14 Therefore, we hypothesized that plaque thrombogenicity may be greatly influenced by the occurrence of apoptotic cell death.
We detected substantial expression of TF in TUNEL-positive areas of plaques. Although the TUNEL method, in some instances, may reveal processes other than apoptosis,30 we have adapted the technique to enhance its specificity for the detection of apoptosis. In addition, we have previously shown6 that in the human atherosclerotic plaque, TUNEL-positive cells colocalize with caspase 3, which is characteristic of apoptosis.33
Extracellular expression of TF in the apoptotic areas suggested to us that it was probably released in microparticles during cell death. The finding of a close association between TF expression and apoptosis in acellular and cellular regions of atherosclerotic plaques suggested the possibility of synergy between TF and apoptotic cell membranes, rendering them highly thrombogenic.
To confirm this hypothesis, we searched for the presence of shed membrane particles with procoagulant potential in atherosclerotic plaques. In this study, we show that a large proportion of phosphatidylserine-bearing microparticles is produced in the atherosclerotic plaque. A number of arguments indicate that these microparticles most likely originated from apoptotic cells: (1) Several groups have shown that apoptosis occurs in the atherosclerotic plaque and may contribute to the development of the acellular lipid core.1 2 3 4 5 6 7 30 (2) Stimuli, like pro-inflammatory cytokines, that lead to cell death in the atherosclerotic plaque are potent inducers of apoptosis,34 and TUNEL-positive labeling in the plaque is highly associated with caspase expression,3 6 leading to the suggestion that necrosis in the plaque is a late secondary process due, in part, to the accumulation of unremoved apoptotic bodies. (3) We have previously shown29 that phosphatidylserine-bearing microparticles stem from surface blebs of apoptotic cells and their amount is correlated to the extent of apoptosis. (4) Phosphatidylserine exposure on the external layer of the cell membrane and shedding of membrane microparticles are early events of apoptosis and are produced even when secondary necrosis does not occur.
Interestingly, we found that these plaque-derived apoptotic microparticles account for almost all the TF activity of the plaque extracts, indicating a direct causal relationship between their presence and TF activity. This suggests that shed membrane apoptotic microparticles may play a major role in the initiation of the coagulation cascade. On the other hand, most of these microparticles originated from macrophages and lymphocytes that are known to be abundant at sites of plaque rupture.35 36 37 We therefore propose that apoptotic death of a proportion of these cells may greatly enhance the thrombus formation accelerating vessel occlusion and could lead to acute infarction.
In addition to their direct effect in promotion and amplification of the coagulation cascade, the apoptotic particles bearing CD11a may also act in a variety of intercellular adhesion processes and may be responsible for dissemination of the procoagulant potential to sites remote from the microenvironment of their formation.14 They may also provide the substrate for secretory phospholipase A2, leading to the generation of lysophosphatidic acid, a potent mediator of the inflammatory reaction and a potent platelet agonist.38 Furthermore, such microparticles may play an important role in transcellular lipid metabolism by their concentrated delivery of bioactive lipids.39
Once plaque material is exposed to circulating blood after plaque rupture or erosion, vascular thrombosis may ensue and may culminate in vascular occlusion, precipitating acute ischemic syndromes.40 Procoagulant potential of the exposed material is therefore a key determinant of plaque thrombogenicity and hence of the extent of vascular thrombosis and luminal narrowing. Our results provide strong evidence that apoptotic cell death in the atherosclerotic plaque is a major determinant of plaque thrombogenicity and could offer novel therapeutic strategies for preventing thrombus formation on plaque rupture.
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Acknowledgments |
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This work was supported by grant Caisse Nationale d'Assurance Maladie des Travailleurs Salariés (CNAMTS)/Institut National de la Santé et la Recherche Médicale (INSERM) 4API12, La Fondation de France and Programme Hospitalier de Recherche Clinique 1996.
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Footnotes |
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Correspondence: Alain Tedgui, PhD, INSERM U 141, 41 boulevard de la Chapelle, 75475 Paris Cedex 10, France.
Received July 13, 1998; revision received September 23, 1998; accepted October 9, 1998.
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 A. S. Leroyer, P.-E. Rautou, J.-S. Silvestre, Y. Castier, G. Leseche, C. Devue, M. Duriez, R. P. Brandes, E. Lutgens, A. Tedgui, et al. CD40 Ligand+ Microparticles From Human Atherosclerotic Plaques Stimulate Endothelial Proliferation and Angiogenesis: A Potential Mechanism for Intraplaque Neovascularization J. Am. Coll. Cardiol., October 14, 2008; 52(16): 1302 - 1311. [Abstract] [Full Text] [PDF]
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H. Ait-Oufella, V. Pouresmail, T. Simon, O. Blanc-Brude, K. Kinugawa, R. Merval, G. Offenstadt, G. Leseche, P. L. Cohen, A. Tedgui, et al. Defective Mer Receptor Tyrosine Kinase Signaling in Bone Marrow Cells Promotes Apoptotic Cell Accumulation and Accelerates Atherosclerosis Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1429 - 1431. [Abstract] [Full Text] [PDF]
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S. J. Germain, G. P. Sacks, S. R. Soorana, I. L. Sargent, and C. W. Redman Systemic Inflammatory Priming in Normal Pregnancy and Preeclampsia: The Role of Circulating Syncytiotrophoblast Microparticles J. Immunol., May 1, 2007; 178(9): 5949 - 5956. [Abstract] [Full Text] [PDF]
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O. P. Blanc-Brude, E. Teissier, Y. Castier, G. Leseche, A.-P. Bijnens, M. Daemen, B. Staels, Z. Mallat, and A. Tedgui IAP Survivin Regulates Atherosclerotic Macrophage Survival Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 901 - 907. [Abstract] [Full Text] [PDF]
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 D. M. Schrijvers, G. R.Y. De Meyer, A. G. Herman, and W. Martinet Phagocytosis in atherosclerosis: Molecular mechanisms and implications for plaque progression and stability Cardiovasc Res, February 1, 2007; 73(3): 470 - 480. [Abstract] [Full Text] [PDF]
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O. Morel, F. Toti, B. Hugel, B. Bakouboula, L. Camoin-Jau, F. Dignat-George, and J.-M. Freyssinet Procoagulant Microparticles: Disrupting the Vascular Homeostasis Equation? Arterioscler Thromb Vasc Biol, December 1, 2006; 26(12): 2594 - 2604. [Abstract] [Full Text] [PDF]
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G. Chironi, A. Simon, B. Hugel, M. Del Pino, J. Gariepy, J.-M. Freyssinet, and A. Tedgui Circulating Leukocyte-Derived Microparticles Predict Subclinical Atherosclerosis Burden in Asymptomatic Subjects Arterioscler Thromb Vasc Biol, December 1, 2006; 26(12): 2775 - 2780. [Abstract] [Full Text] [PDF]
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 M. C. Martinez, F. Larbret, F. Zobairi, J. Coulombe, N. Debili, W. Vainchenker, M. Ruat, and J.-M. Freyssinet Transfer of differentiation signal by membrane microvesicles harboring hedgehog morphogens Blood, November 1, 2006; 108(9): 3012 - 3020. [Abstract] [Full Text] [PDF]
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A. Klein, V. Deckert, M. Schneider, F. Dutrillaux, A. Hammann, A. Athias, N. Le Guern, J.-P. Pais de Barros, C. Desrumaux, D. Masson, et al. {alpha}-Tocopherol Modulates Phosphatidylserine Externalization in Erythrocytes: Relevance in Phospholipid Transfer Protein-Deficient Mice Arterioscler Thromb Vasc Biol, September 1, 2006; 26(9): 2160 - 2167. [Abstract] [Full Text] [PDF]
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Z. Touat, V. Ollivier, J. Dai, M.-G. Huisse, A. Bezeaud, U. Sebbag, T. Palombi, P. Rossignol, O. Meilhac, M.-C. Guillin, et al. Renewal of Mural Thrombus Releases Plasma Markers and Is Involved in Aortic Abdominal Aneurysm Evolution Am. J. Pathol., March 1, 2006; 168(3): 1022 - 1030. [Abstract] [Full Text] [PDF]
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A. Tesse, M. C. Martinez, B. Hugel, K. Chalupsky, C. D. Muller, F. Meziani, D. Mitolo-Chieppa, J.-M. Freyssinet, and R. Andriantsitohaina Upregulation of Proinflammatory Proteins Through NF-{kappa}B Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity Arterioscler Thromb Vasc Biol, December 1, 2005; 25(12): 2522 - 2527. [Abstract] [Full Text] [PDF]
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I. Tabas Consequences and Therapeutic Implications of Macrophage Apoptosis in Atherosclerosis: The Importance of Lesion Stage and Phagocytic Efficiency Arterioscler Thromb Vasc Biol, November 1, 2005; 25(11): 2255 - 2264. [Abstract] [Full Text] [PDF]
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Z. Mallat, Ph. G. Steg, J. Benessiano, M.-L. Tanguy, K. A. Fox, J.-P. Collet, O. H. Dabbous, P. Henry, K. F. Carruthers, A. Dauphin, et al. Circulating Secretory Phospholipase A2 Activity Predicts Recurrent Events in Patients With Severe Acute Coronary Syndromes J. Am. Coll. Cardiol., October 4, 2005; 46(7): 1249 - 1257. [Abstract] [Full Text] [PDF]
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V. Fuster, P. R. Moreno, Z. A. Fayad, R. Corti, and J. J. Badimon Atherothrombosis and High-Risk Plaque: Part I: Evolving Concepts J. Am. Coll. Cardiol., September 20, 2005; 46(6): 937 - 954. [Abstract] [Full Text] [PDF]
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C. M. Boulanger and A. Tedgui Dying for attention: Microparticles and angiogenesis Cardiovasc Res, July 1, 2005; 67(1): 1 - 3. [Full Text] [PDF]
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D. M. Schrijvers, G. R.Y. De Meyer, M. M. Kockx, A. G. Herman, and W. Martinet Phagocytosis of Apoptotic Cells by Macrophages Is Impaired in Atherosclerosis Arterioscler Thromb Vasc Biol, June 1, 2005; 25(6): 1256 - 1261. [Abstract] [Full Text] [PDF]
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H. Koga, S. Sugiyama, K. Kugiyama, K. Watanabe, H. Fukushima, T. Tanaka, T. Sakamoto, M. Yoshimura, H. Jinnouchi, and H. Ogawa Elevated Levels of VE-Cadherin-Positive Endothelial Microparticles in Patients With Type 2 Diabetes Mellitus and Coronary Artery Disease J. Am. Coll. Cardiol., May 17, 2005; 45(10): 1622 - 1630. [Abstract] [Full Text] [PDF]
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S. M. Day, J. L. Reeve, B. Pedersen, D. M Farris, D. D. Myers, M. Im, T. W. Wakefield, N. Mackman, and W. P. Fay Macrovascular thrombosis is driven by tissue factor derived primarily from the blood vessel wall Blood, January 1, 2005; 105(1): 192 - 198. [Abstract] [Full Text] [PDF]
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A. C. Ferreira, A. A. Peter, A. J. Mendez, J. J. Jimenez, L. M. Mauro, J. A. Chirinos, R. Ghany, S. Virani, S. Garcia, L. L. Horstman, et al. Postprandial Hypertriglyceridemia Increases Circulating Levels of Endothelial Cell Microparticles Circulation, December 7, 2004; 110(23): 3599 - 3603. [Abstract] [Full Text] [PDF]
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M. L. Rossi, N. Marziliano, P. A. Merlini, E. Bramucci, U. Canosi, G. Belli, D. Z. Parenti, P. M. Mannucci, and D. Ardissino Different Quantitative Apoptotic Traits in Coronary Atherosclerotic Plaques From Patients With Stable Angina Pectoris and Acute Coronary Syndromes Circulation, September 28, 2004; 110(13): 1767 - 1773. [Abstract] [Full Text] [PDF]
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L. Mazzolai, M. A. Duchosal, M. Korber, K. Bouzourene, J. F. Aubert, H. Hao, V. Vallet, H. R. Brunner, J. Nussberger, G. Gabbiani, et al. Endogenous Angiotensin II Induces Atherosclerotic Plaque Vulnerability and Elicits a Th1 Response in ApoE-/- Mice Hypertension, September 1, 2004; 44(3): 277 - 282. [Abstract] [Full Text] [PDF]
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Y. Li, M. Ge, L. Ciani, G. Kuriakose, E. J. Westover, M. Dura, D. F. Covey, J. H. Freed, F. R. Maxfield, J. Lytton, et al. Enrichment of Endoplasmic Reticulum with Cholesterol Inhibits Sarcoplasmic-Endoplasmic Reticulum Calcium ATPase-2b Activity in Parallel with Increased Order of Membrane Lipids: IMPLICATIONS FOR DEPLETION OF ENDOPLASMIC RETICULUM CALCIUM STORES AND APOPTOSIS IN CHOLESTEROL-LOADED MACROPHAGES J. Biol. Chem., August 27, 2004; 279(35): 37030 - 37039. [Abstract] [Full Text] [PDF]
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N. Mackman Role of Tissue Factor in Hemostasis, Thrombosis, and Vascular Development Arterioscler Thromb Vasc Biol, June 1, 2004; 24(6): 1015 - 1022. [Abstract] [Full Text] [PDF]
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R. Hutter, C. Valdiviezo, B. V. Sauter, M. Savontaus, I. Chereshnev, F. E. Carrick, G. Bauriedel, B. Luderitz, J. T. Fallon, V. Fuster, et al. Caspase-3 and Tissue Factor Expression in Lipid-Rich Plaque Macrophages: Evidence for Apoptosis as Link Between Inflammation and Atherothrombosis Circulation, April 27, 2004; 109(16): 2001 - 2008. [Abstract] [Full Text] [PDF]
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S. Martin, A. Tesse, B. Hugel, M. C. Martinez, O. Morel, J.-M. Freyssinet, and R. Andriantsitohaina Shed Membrane Particles From T Lymphocytes Impair Endothelial Function and Regulate Endothelial Protein Expression Circulation, April 6, 2004; 109(13): 1653 - 1659. [Abstract] [Full Text] [PDF]
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H. Kobayashi, N. Ouchi, S. Kihara, K. Walsh, M. Kumada, Y. Abe, T. Funahashi, and Y. Matsuzawa Selective Suppression of Endothelial Cell Apoptosis by the High Molecular Weight Form of Adiponectin Circ. Res., March 5, 2004; 94 (4): e27 - e31. [Abstract] [Full Text] [PDF]
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M. J. VanWijk, E. VanBavel, A. Sturk, and R. Nieuwland Microparticles in cardiovascular diseases Cardiovasc Res, August 1, 2003; 59(2): 277 - 287. [Abstract] [Full Text] [PDF]
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P. K. Shah Mechanisms of plaque vulnerability and rupture J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 15S - 22S. [Abstract] [Full Text] [PDF]
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R. A. Preston, W. Jy, J. J. Jimenez, L. M. Mauro, L. L. Horstman, M. Valle, G. Aime, and Y. S. Ahn Effects of Severe Hypertension on Endothelial and Platelet Microparticles Hypertension, February 1, 2003; 41(2): 211 - 217. [Abstract] [Full Text] [PDF]
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J. Blanc, M.C. Alves-Guerra, B. Esposito, S. Rousset, P. Gourdy, D. Ricquier, A. Tedgui, B. Miroux, and Z. Mallat Protective Role of Uncoupling Protein 2 in Atherosclerosis Circulation, January 28, 2003; 107(3): 388 - 390. [Abstract] [Full Text] [PDF]
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M. Valgimigli, L. Agnoletti, S. Curello, L. Comini, G. Francolini, F. Mastrorilli, E. Merli, R. Pirani, G. Guardigli, P. G. Grigolato, et al. Serum From Patients With Acute Coronary Syndromes Displays a Proapoptotic Effect on Human Endothelial Cells: A Possible Link to Pan-Coronary Syndromes Circulation, January 21, 2003; 107(2): 264 - 270. [Abstract] [Full Text] [PDF]
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M. Diamant, R. Nieuwland, R. F. Pablo, A. Sturk, J. W.A. Smit, and J. K. Radder Elevated Numbers of Tissue-Factor Exposing Microparticles Correlate With Components of the Metabolic Syndrome in Uncomplicated Type 2 Diabetes Mellitus Circulation, November 5, 2002; 106(19): 2442 - 2447. [Abstract] [Full Text] [PDF]
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B. Feng and I. Tabas ABCA1-mediated Cholesterol Efflux Is Defective in Free Cholesterol-loaded Macrophages. MECHANISM INVOLVES ENHANCED ABCA1 DEGRADATION IN A PROCESS REQUIRING FULL NPC1 ACTIVITY J. Biol. Chem., November 1, 2002; 277(45): 43271 - 43280. [Abstract] [Full Text] [PDF]
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Q. Xu Role of Heat Shock Proteins in Atherosclerosis Arterioscler Thromb Vasc Biol, October 1, 2002; 22(10): 1547 - 1559. [Abstract] [Full Text] [PDF]
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V. Balasubramanian, E. Grabowski, A. Bini, and Y. Nemerson Platelets, circulating tissue factor, and fibrin colocalize in ex vivo thrombi: real-time fluorescence images of thrombus formation and propagation under defined flow conditions Blood, September 26, 2002; 100(8): 2787 - 2792. [Abstract] [Full Text] [PDF]
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R. Kraemer Reduced Apoptosis and Increased Lesion Development in the Flow-Restricted Carotid Artery of p75NTR-Null Mutant Mice Circ. Res., September 20, 2002; 91(6): 494 - 500. [Abstract] [Full Text] [PDF]
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Y. Nemerson A Simple Experiment and a Weakening Paradigm: The Contribution of Blood to Propensity for Thrombus Formation Arterioscler Thromb Vasc Biol, September 1, 2002; 22(9): 1369 - 1369. [Full Text] [PDF]
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R. Gonzalez-Conejero, J. Corral, V. Roldan, C. Martinez, F. Marin, J. Rivera, J. A. Iniesta, M. L. Lozano, P. Marco, and V. Vicente A common polymorphism in the annexin V Kozak sequence (-1C>T) increases translation efficiency and plasma levels of annexin V, and decreases the risk of myocardial infarction in young patients Blood, August 28, 2002; 100(6): 2081 - 2086. [Abstract] [Full Text] [PDF]
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F. Sabatier, V. Roux, F. Anfosso, L. Camoin, J. Sampol, and F. Dignat-George Interaction of endothelial microparticles with monocytic cells in vitro induces tissue factor-dependent procoagulant activity Blood, May 13, 2002; 99(11): 3962 - 3970. [Abstract] [Full Text] [PDF]
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D. Bonderman, A. Teml, J. Jakowitsch, C. Adlbrecht, M. Gyongyosi, W. Sperker, H. Lass, W. Mosgoeller, D. H. Glogar, P. Probst, et al. Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque Blood, April 15, 2002; 99(8): 2794 - 2800. [Abstract] [Full Text] [PDF]
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M. H. Yamani, C. S. Masri, N. B. Ratliff, M. Bond, R. C. Starling, E. M. Tuzcu, P. M. McCarthy, and J. B. Young The role of vitronectin receptor ({alpha}v{beta}3) and tissue factor in the pathogenesis of transplant coronary vasculopathy J. Am. Coll. Cardiol., March 6, 2002; 39(5): 804 - 810. [Abstract] [Full Text] [PDF]
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A. H.M Moons, M. Levi, and R. J.G Peters Tissue factor and coronary artery disease Cardiovasc Res, February 1, 2002; 53(2): 313 - 325. [Abstract] [Full Text] [PDF]
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J. Huber, A. Vales, G. Mitulovic, M. Blumer, R. Schmid, J. L. Witztum, B. R. Binder, and N. Leitinger Oxidized Membrane Vesicles and Blebs From Apoptotic Cells Contain Biologically Active Oxidized Phospholipids That Induce Monocyte-Endothelial Interactions Arterioscler Thromb Vasc Biol, January 1, 2002; 22(1): 101 - 107. [Abstract] [Full Text] [PDF]
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P. M. Yao and I. Tabas Free Cholesterol Loading of Macrophages Is Associated with Widespread Mitochondrial Dysfunction and Activation of the Mitochondrial Apoptosis Pathway J. Biol. Chem., November 2, 2001; 276(45): 42468 - 42476. [Abstract] [Full Text] [PDF]
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A. H. M. Hassan, I. M. Lang, M. Ignatescu, R. Ullrich, D. Bonderman, P. Wexberg, F. Weidinger, and H. D. Glogar Increased intimal apoptosis in coronary atherosclerotic vessel segments lacking compensatory enlargement J. Am. Coll. Cardiol., November 1, 2001; 38(5): 1333 - 1339. [Abstract] [Full Text] [PDF]
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Z. Mallat, A. Corbaz, A. Scoazec, P. Graber, S. Alouani, B. Esposito, Y. Humbert, Y. Chvatchko, and A. Tedgui Interleukin-18/Interleukin-18 Binding Protein Signaling Modulates Atherosclerotic Lesion Development and Stability Circ. Res., September 28, 2001; 89 (7): e41 - e45. [Abstract] [Full Text] [PDF]
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Z. Mallat and A. Tedgui Current Perspective on the Role of Apoptosis in Atherothrombotic Disease Circ. Res., May 25, 2001; 88(10): 998 - 1003. [Abstract] [Full Text] [PDF]
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M. R. Bennett Reactive Oxygen Species and Death : Oxidative DNA Damage in Atherosclerosis Circ. Res., April 13, 2001; 88(7): 648 - 650. [Full Text] [PDF]
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F. D. Kolodgie, J. Narula, A. P. Burke, N. Haider, A. Farb, Y. Hui-Liang, J. Smialek, and R. Virmani Localization of Apoptotic Macrophages at the Site of Plaque Rupture in Sudden Coronary Death Am. J. Pathol., October 1, 2000; 157(4): 1259 - 1268. [Abstract] [Full Text] [PDF]
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M. M. Kockx, C. Seye, G. R. Y. De Meyer, M. W. M. Knaapen, M. Aikawa, S. J. Voglic, S. Sugiyama, E. Rabkin, P. Libby, M. B. Taubman, et al. Decreased Apoptosis and Tissue Factor Expression After Lipid Lowering Response Circulation, September 26, 2000; 102 (13): e99 - e99. [Full Text] [PDF]
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A. Tedgui and Z. Mallat Smooth Muscle Cells : Another Source of Tissue Factor-Containing Microparticles in Atherothrombosis? Circ. Res., July 21, 2000; 87(2): 81 - 82. [Full Text] [PDF]
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A. D. Schecter, B. Spirn, M. Rossikhina, P. L. A. Giesen, V. Bogdanov, J. T. Fallon, E. A. Fisher, L. M. Schnapp, Y. Nemerson, and M. B. Taubman Release of Active Tissue Factor by Human Arterial Smooth Muscle Cells Circ. Res., July 21, 2000; 87(2): 126 - 132. [Abstract] [Full Text] [PDF]
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O. Tricot, Z. Mallat, C. Heymes, J. Belmin, G. Leseche, and A. Tedgui Relation Between Endothelial Cell Apoptosis and Blood Flow Direction in Human Atherosclerotic Plaques Circulation, May 30, 2000; 101(21): 2450 - 2453. [Abstract] [Full Text] [PDF]
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E. Arnaud, V. Barbalat, V. Nicaud, F. Cambien, A. Evans, C. Morrison, D. Arveiler, G. Luc, J.-B. Ruidavets, J. Emmerich, et al. Polymorphisms in the 5' Regulatory Region of the Tissue Factor Gene and the Risk of Myocardial Infarction and Venous Thromboembolism : The ECTIM and PATHROS Studies Arterioscler Thromb Vasc Biol, March 1, 2000; 20(3): 892 - 898. [Abstract] [Full Text] [PDF]
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Z. Mallat, H. Benamer, B. Hugel, J. Benessiano, P. G. Steg, J.-M. Freyssinet, and A. Tedgui Elevated Levels of Shed Membrane Microparticles With Procoagulant Potential in the Peripheral Circulating Blood of Patients With Acute Coronary Syndromes Circulation, February 29, 2000; 101(8): 841 - 843. [Abstract] [Full Text] [PDF]
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R. Nieuwland, R. J. Berckmans, S. McGregor, A. N. Boing, F. P. H. Th. M. Romijn, R. G. J. Westendorp, C. E. Hack, and A. Sturk Cellular origin and procoagulant properties of microparticles in meningococcal sepsis Blood, February 1, 2000; 95(3): 930 - 935. [Abstract] [Full Text] [PDF]
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W. L van Heerde, S. Robert-Offerman, E. Dumont, L. Hofstra, P. A Doevendans, J. F.M Smits, M. J.A.P Daemen, and C. P.M Reutelingsperger Markers of apoptosis in cardiovascular tissues: focus on Annexin V Cardiovasc Res, February 1, 2000; 45(3): 549 - 559. [Abstract] [Full Text] [PDF]
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M. M Kockx and A. G Herman Apoptosis in atherosclerosis: beneficial or detrimental? Cardiovasc Res, February 1, 2000; 45(3): 736 - 746. [Abstract] [Full Text] [PDF]
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N. J. McCarthy and M. Bennett The regulation of vascular smooth muscle cell apoptosis Cardiovasc Res, February 1, 2000; 45(3): 747 - 755. [Abstract] [Full Text] [PDF]
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Z. Mallat, S. Besnard, M. Duriez, V. Deleuze, F. Emmanuel, M. F. Bureau, F. Soubrier, B. Esposito, H. Duez, C. Fievet, et al. Protective Role of Interleukin-10 in Atherosclerosis Circ. Res., October 15, 1999; 85 (8): e17 - e24. [Abstract] [Full Text] [PDF]
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M. Mesri and D. C. Altieri Leukocyte Microparticles Stimulate Endothelial Cell Cytokine Release and Tissue Factor Induction in a JNK1 Signaling Pathway J. Biol. Chem., August 13, 1999; 274(33): 23111 - 23118. [Abstract] [Full Text] [PDF]
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J.-R. Nofer, B. Levkau, I. Wolinska, R. Junker, M. Fobker, A. von Eckardstein, U. Seedorf, and G. Assmann Suppression of Endothelial Cell Apoptosis by High Density Lipoproteins (HDL) and HDL-associated Lysosphingolipids J. Biol. Chem., September 7, 2001; 276(37): 34480 - 34485. [Abstract] [Full Text] [PDF]
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V. A. Patel, Q.-J. Zhang, K. Siddle, M. A. Soos, M. Goddard, P. L. Weissberg, and M. R. Bennett Defect in Insulin-Like Growth Factor-1 Survival Mechanism in Atherosclerotic Plaque-Derived Vascular Smooth Muscle Cells Is Mediated by Reduced Surface Binding and Signaling Circ. Res., May 11, 2001; 88(9): 895 - 902. [Abstract] [Full Text] [PDF]
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