© 1997 American Heart Association, Inc.
Articles |
Hemodynamic Regulation of Tumor Necrosis Factor-
Gene and Protein Expression in Adult Feline Myocardium
From the Cardiology and Geriatric Sections of the Department of Medicine, Veterans Administration Medical Center, and Baylor College of Medicine, Houston, Tex.
Correspondence to Douglas L. Mann, MD, Cardiology Research (151C), Room 234, Building 110, VA Medical Center, 2002 Holcombe Blvd, Houston, TX 77030. E-mail dmann{at}bcm.tmc.edu
Abstract Tumor necrosis factor- (TNF-) mRNA and
protein biosynthesis were examined in adult feline
myocardium in the presence and absence of superimposed
hemodynamic pressure overloading. A brief period of
hemodynamic pressure overloading ex vivo resulted in de
novo TNF- mRNA expression within 30 minutes and de novo TNF-
protein production within 60 minutes; neither TNF- mRNA nor
protein was detected in hearts perfused at normal perfusion pressures.
Moreover, TNF- mRNA and protein biosynthesis were observed in
myocyte and nonmyocyte cell types in the pressure-overloaded
hearts. To determine whether a simple passive stretch of the
myocardium was a sufficient stimulus for TNF-
biosynthesis, we examined TNF- mRNA expression in stretched and
unstretched papillary muscles. This study showed that myocardial
stretch was a sufficient stimulus for the induction of TNF- mRNA
biosynthesis. The functional significance of the intramyocardial
production of TNF- was determined by examining cell motion
in isolated contracting cardiac myocytes treated with
superfusates from pressure-overloaded and control hearts. These
studies showed that cell motion was depressed in myocytes treated with
superfusates from the pressure-overloaded hearts but was normal
with the superfusates from the control hearts. Finally,
hemodynamic pressure overloading in vivo under
physiological conditions was also shown to result
in de novo intramyocardial TNF- mRNA biosynthesis. In conclusion,
this study constitutes the initial demonstration that the adult
mammalian myocardium elaborates biologically active
TNF-, both ex vivo and in vivo, in response to
hemodynamic pressure overloading.
Key Words: tumor necrosis factor- • pressure overload • gene expression • myocyte
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