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2004 JAN 1 - (NewsRx.com & NewsRx.net) -- Hypoxic myocytes produce growth factor that stimulates COX-2 production.
According to published research from the United States, "there is increasing evidence that cyclooxygenase (COX)-2 possess both angiogenic and cardioprotective properties. We examined the effects of hypoxic cardiac myocytes (H9c2 cells) on COX-2 expression in human umbilical vein endothelial cells (HUVECs) to determine the pathway involved in COX-2 regulation. The medium from hypoxic (
"HMCM induced a transient increase of COX-2 mRNA expression at 1 and 3 hours without affecting the COX-1 mRNA level. A similar effect also observed in HMCM from cultured primary cardiac myocytes (rat neonatal cardiac myocytes). The increased COX-2 mRNA was associated with a time-dependent increase in COX-2 protein expression," reported G.F. Wu and colleagues, Harvard University, School of Medicine.
"COX-2 was significantly induced by VEGF (4.86[+ or -]1.03-fold) and IL-1beta; (3.93[+ or -]0.89-fold) and slightly increased by TNF-alpha; but not by FGF2, IGF-1, or PDGFs. Analysis of proteins secreted in HMCM showed increased levels of VEGF but not IL-1beta; or TNF-alpha;. The HMCM-induced COX-2 expression was inhibited by the addition of an anti-VEGF neutralizing antibody. VEGF induced endothelial cell COX-2 expression by both increasing COX-2 transcription and prolonging the COX-2 mRNA half-life," scientists said.
"Furthermore, staurosporine, a nonselective PKC inhibitor, prevented the induction of VEGF by hypoxia. Both a selective PKC-alpha; and -beta; inhibitor and an inducible nitric oxide ...
Source: HighBeam Research, Hypoxic myocytes produce growth factor that stimulates COX-2...