PMID: 11327337May 1, 2001Paper

Inhibition of rat cardiac fibroblast growth by cAMP--but not by cGMP-dependent protein kinase

Basic Research in Cardiology
U MarienfeldAndreas Simm

Abstract

Cardiac fibroblasts play a critical role in the process of pathophysiological cardiac hypertrophy as the cell type responsible for fibrosis. Whereas many growth factors and hormones are thought to be involved, possible crosstalks between signal transduction pathways are not well defined. Therefore we investigated the influence of cAMP- and cGMP-dependent protein kinases (cAK, cGK) on platelet derived growth factor (PDGF) stimulated growth of primary cardiac fibroblasts from adult rats. We show here that PDGF-BB induced cell proliferation can be inhibited by activation of the endogenous cAK directly via the cAMP analog 5,6-DCL-cBIMPS as well as indirectly via the cAMP-elevating receptor agonist prostaglandin-E1 (PGE1). In contrast, activation of the endogenous cGK-I has no influence on cardiac fibroblast cell growth. The strength of the proliferation inhibition is dependent on the time course of cAK activation, i.e., longer activation with the cAMP analog results in stronger proliferation inhibition. No significant influence of cAK or cGK-I on Akt activation or on the short-term activation of the MAPK cascade was observed. In contrast, 5,6-DCI-cBIMPS treatment of cardiac fibroblasts causes an inhibition of long-term MAPK phospho...Continue Reading

Citations

Nov 18, 2014·The Journal of Clinical Investigation·Yassine SassiStefan Engelhardt
Aug 24, 2007·Biochemical Pharmacology·Leonor Sterin-BordaEnri Borda
Oct 20, 2006·Nitric Oxide : Biology and Chemistry·Anna-Louise M Cook, John M Haynes
Nov 23, 2005·Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology·César FurlánEnri Borda
May 11, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Donald D DoyleH Clive Palfrey

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