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Articles in PresS, published online ahead of print November 8, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00436.2001
Submitted on May 22, 2001
Accepted on November 5, 2001
, IL-6, and IGF-1 by graded mechanical stress in normal rat myocardium
1 Medicina Clinica, Scienze Cardiovascilari ed Immunologiche, Facolta di Medicina e Chirurgia, Universita degli Studi di Napoli, Napoli, Italy
2 Scienze Biomorfologiche e Funzionali, Sezione di Anatomia Patologica e Citopatologia, Facolta di Medicina e Chirurgia, Universita degli Studi di Napoli, Napoli, Italy
3 Medicina Sperimentale e Clinica, Facolta di Medicina e Chirurgia, Universita degli Studi di Catanzaro, Catanzaro, Italy
4 Biologia e Patologia Cellulare e Molecolare, Facolta di Medicina e Chirurgia, Universita degli Studi di Napoli, Napoli, Italy
* To whom correspondence should be addressed. E-mail: eapalmieri{at}ciaoweb.it.
An isovolumic normal rat heart Langendorff model was used to examine the effects of moderate (15 mmHg) and severe (35 mmHg) mechanical stretch on the time course (from 0 to 60 min) of myocardial expression of tumor necrosis factor (TNF)-, interleukin (IL)-6, insulin-like growth factor (IGF)-1, and of their cognate receptors. After 10 min of moderate stretch, TNF- was de novo expressed, whereas constitutive IL-6 and IGF-1 levels were slightly upregulated; no further changes occurred up to 60 min. By comparison, severe stretch resulted in a higher and progressive increase in TNF-, IL-6, and IGF-1 expression up to 20 minutes. After 20 minutes, while TNF- expression further increased, IL-6 and IGF-I levels progressively reduced to values lower than those observed under moderate stretch and in unstretched (5 mmHg) control myocardium (IL-6). Mechanical stretch did not alter significantly the cognate receptors' expression. Indeed, TNF- receptor (p55) tended to be progressively upregulated under severe stretch over time. The current data provide the first demonstration that TNF-, IL-6, and IGF-1 ligand-receptor systems are differentially expressed within normal rat myocardium in response to graded mechanical stretch. Such findings may have potential implications with regard to compensatory hypertrophy and failure.
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