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Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective PhenotypesA Speculative Synthesis
Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King and Roger P. Simon

Stroke. 2007;38:680-685, originally published January 29, 2007
https://doi.org/10.1161/01.STR.0000251444.56487.4c

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Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon

Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c

Figure 1. LPS and ischemic preconditioning alter the genomic response to stroke. Venn diagrams showing the percent of overlap in gene regulation 3 and...Show More

Figure 1. LPS and ischemic preconditioning alter the genomic response to stroke. Venn diagrams showing the percent of overlap in gene regulation 3 and 24 hours after stroke in mice preconditioned with LPS (5 μg) or brief ischemia (15 minutes) vs control animals subjected to stroke without prior preconditioning. Preconditioning plus stroke represented by the yellow circles; stroke alone represented by the blue circles; overlap shown in green.Show Less
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Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon

Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c

Figure 2. Ischemic preconditioning suppresses expression of genes involved in cellular metabolism and homeostasis. Ischemic preconditioning before str...Show More

Figure 2. Ischemic preconditioning suppresses expression of genes involved in cellular metabolism and homeostasis. Ischemic preconditioning before stroke modulates the expression of a unique subset of genes that influence metabolism or transport/channels. Gene regulation is displayed from samples taken 24 hours after stroke in the presence or absence of ischemic preconditioning. Gene expression: red indicates increased expression; green indicates decreased expression; gray indicates no change in expression. Genes were assigned to Biological Function categories based on the Gene Consortium database and literature review. HDAC5 indicates histone deacetylase 5; Ptgds, prostaglandin D2 synthase; GluR1, glutamate receptor ionotropic AMPA1; GluR3, glutamate receptor ionotropic AMPA3; KA2, glutamate receptor ionotropic kainate5 γ2; Atpa1, ATPase Na+/K+ transporting α1 polypeptide.Show Less
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Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon

Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c

Figure 3. LPS preconditioning alters the inflammatory response to stroke injury by suppressing pro-inflammatory and increasing anti-inflammatory media...Show More

Figure 3. LPS preconditioning alters the inflammatory response to stroke injury by suppressing pro-inflammatory and increasing anti-inflammatory mediators. LPS preconditioning before stroke modulates the expression of a unique subset of genes associated with defense responses. Gene regulation is displayed from samples taken 24 hours after stroke in the presence or absence of LPS preconditioning. Gene expression: red indicates increased expression; green indicates decreased expression; gray indicates no change in expression. The shaded red area represents genes associated with type I interferons. Genes were assigned to Biological Function categories based on the Gene Consortium database and literature review. IL6 indicates interleukin 6; Mip1a, macrophage inflammatory protein 1α; IL1r, interleukin 1 receptor; Traf6, Tnf receptor-associated factor 6.Show Less
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Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon

Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c

Figure 4. Osteopontin does not induce unique gene regulation in response to stroke. Venn diagram showing unique gene regulation (percentage) 24 hours...Show More

Figure 4. Osteopontin does not induce unique gene regulation in response to stroke. Venn diagram showing unique gene regulation (percentage) 24 hours after stroke in mice treated with osteopontin vs mice given a stroke without osteopontin treatment. Osteopontin plus stroke and overlap shown in the green circle and stroke alone represented by the blue circle. Osteopontin treatment reduced the number of genes with changes in expression by 4-fold.Show Less
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Endotoxin Preconditioning Prevents Cellular Inflammatory Response During Ischemic Neuroprotection in Mice
Holly L. Rosenzweig, Nikola S. Lessov, David C. Henshall, Manabu Minami, Roger P. Simon and Mary P. Stenzel-Poore

Stroke. 2004;35:2576-2581, originally published October 28, 2004
https://doi.org/10.1161/01.STR.0000143450.04438.ae

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Endotoxin Preconditioning Prevents Cellular Inflammatory Response During Ischemic Neuroprotection in Mice
Holly L. Rosenzweig, Nikola S. Lessov, David C. Henshall, Manabu Minami, Roger P. Simon, Mary P. Stenzel-Poore

Stroke November 2004, 35 (11) 2576-2581; DOI: https://doi.org/10.1161/01.STR.0000143450.04438.ae

Figure 1. Effect of LPS preconditioning on infarct size. Mice were pretreated with LPS or s...
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Figure 1. Effect of LPS preconditioning on infarct size. Mice were pretreated with LPS or saline 48 hours before MCAO. Infarcts were assessed 48 hours after MCAO and quantified as percentage area of ischemic hemisphere. Values are mean±SEM; *P<0.05 vs saline treatment; n=12 mice per group.
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Endotoxin Preconditioning Prevents Cellular Inflammatory Response During Ischemic Neuroprotection in Mice
Holly L. Rosenzweig, Nikola S. Lessov, David C. Henshall, Manabu Minami, Roger P. Simon, Mary P. Stenzel-Poore

Stroke November 2004, 35 (11) 2576-2581; DOI: https://doi.org/10.1161/01.STR.0000143450.04438.ae

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TABLE 1. Effect of LPS Preconditioning on No. of CD11b+ Cells in Ischemic Brain Tissue...
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TABLE 1. Effect of LPS Preconditioning on No. of CD11b+ Cells in Ischemic Brain Tissue
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Endotoxin Preconditioning Prevents Cellular Inflammatory Response During Ischemic Neuroprotection in Mice
Holly L. Rosenzweig, Nikola S. Lessov, David C. Henshall, Manabu Minami, Roger P. Simon, Mary P. Stenzel-Poore

Stroke November 2004, 35 (11) 2576-2581; DOI: https://doi.org/10.1161/01.STR.0000143450.04438.ae

Figure 2. Effect of LPS preconditioning on microglial activation in brain after MCAO. Activ...
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Figure 2. Effect of LPS preconditioning on microglial activation in brain after MCAO. Activated microglia populations were quantified by flow cytometry in ischemic and nonischemic brain hemispheres (dashed line) 48 hours after MCAO in LPS-preconditioned mice. A, Representative flow cytometric plot of the ischemic hemisphere of an individual mouse. Arrow indicates activated microglia (CD45-hi and CD11b-hi) present after MCAO but diminished in LPS-preconditioned mice. B, Values are mean percentage of activated microglia of total population±SEM; *P<0.05 vs saline-treated mice; n=8 to 12 mice per group.
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Endotoxin Preconditioning Prevents Cellular Inflammatory Response During Ischemic Neuroprotection in Mice
Holly L. Rosenzweig, Nikola S. Lessov, David C. Henshall, Manabu Minami, Roger P. Simon, Mary P. Stenzel-Poore

Stroke November 2004, 35 (11) 2576-2581; DOI: https://doi.org/10.1161/01.STR.0000143450.04438.ae

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TABLE 2. Effect of LPS Preconditioning on WBC Infiltration in Brain After MCAO in Mice...
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TABLE 2. Effect of LPS Preconditioning on WBC Infiltration in Brain After MCAO in Mice
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