(Circulation. 1995;92:1487-1493.)
© 1995 American Heart Association, Inc.
Articles |
Expression and Functional Significance of Tumor Necrosis Factor Receptors in Human Myocardium
From the Cardiology Section (G.T.-A., S.K., J.L., R.L., D.L.M.), Departments of Medicine and Pathology, Veterans Administration Medical Center and Baylor College of Medicine, Houston, Tex; and the Cardiology Section (R.D.B.), Department of Medicine, University of Colorado (Denver).
Correspondence to Douglas L. Mann, MD, Cardiology Section, VA Medical Center, 2002 Holcombe Blvd, Houston, TX 77030.
Background Tumor necrosis factor–
(TNF-), a
proinflammatory cytokine with potent negative inotropic
properties, is elaborated in septic shock, acute myocarditis,
reperfusion injury, and congestive heart failure. TNF- acts by
binding to two specific receptors: TNFR1 and TNFR2. However, neither
the presence nor the significance of TNF receptors has been studied in
the adult mammalian heart.
Methods and Results In the present study, we showed that the
adult heart expresses mRNA and receptor proteins for TNFR1 and TNFR2.
Moreover, immunohistochemical staining studies localized TNFR1 and
TNFR2 to the cardiac myocyte, providing a potential signaling pathway
for the deleterious effects of TNF-. The functional significance of
the expression of TNFR1 and TNFR2 was explored with the use of a simple
cell motion assay in which we assessed the effect(s) of TNF- mutants
known to bind selectively to human TNFR1 and TNFR2. We showed that the
negative inotropic effect of wild-type TNF- in isolated feline
cardiac myocytes was mimicked by the TNF mutant that binds to TNFR1,
whereas the TNF mutant that binds to TNFR2 had no significant effect on
cell motion.
Conclusions Results of the present study show that the adult
human heart expresses both mRNA and receptor proteins for TNFR1 and
TNFR2; moreover, the negative inotropic effects of TNF- in adult
cardiac myocytes appear to be initiated by activation of TNFR1.
Key Words: tumor necrosis factor • myocardium • myocytes
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