Title: Effects of ERK/P38MAPK pathway on the phenotypic modulation of human umbilical arterial smooth muscle cell
Abstract: Objective To investigate the role and the molecular mechanisms of the ERK and p38 MAPK pathways on the phenotypic modulation of the cultured vascular smooth muscle cells. Methods To establish a steady cell culture model in vitro for vascular smooth muscle cells (VSMC) of human umbilical artery. The HASMC was incubated with DMEM without serum,PDGF-BB(20 ng/ml),PDGF-BB(20 ng/ml)+ PD98059(30 μmol/L)+SB203580(20μmol/L),PDGF-BB(20 ng/ml) + minocycline(15 μmol/L),PDGF-BB(20 ng/ml)+ minocycline(30 μmol/L). The expression of ERK1/2,P-ERK1/2,P38 and P-P38 protein of HASMC was detected by the way of Western Blot. Results The relative expression of P-P38 protein of HASMCs incubated with PDGF-BB(20 ng/ml)+ minocycline(1 5 μmol/L)for 24h,was lower than that of the PDGF-BB(20 ng/ml) group (P0.01). The relative expression of P-ERK1/2,P-P38 protein of HASMCs incubated with PDGF-BB(20 ng/ml)+ minocycline(15 μmol/L),PDGF-BB(20 ng/ml)+ minocycline(30 μmol/L)for 24 h,was respectively lower than that of the PDGF-BB(20ng/ml) group,revealing that minocycline down-regulated P-ERK1/2,P-P38 protein of HASMC significantly (P0.01). Conclusions (1)PDGF-BB activated ERK/P38MAPK pathways to induced de-differentiation of the HASMC. When the ERK/P38MAPK pathways were simultaneously blocked by their specific inhibitors,PDGF-BB in turn initiated to maintain the differentiated SMC phenotype.( 2) This result suggests that the inhibitory effect of minocycline on HASMC dedifferentiation induced by PDGF-BB was not caused by the cytotoxicity caused by minocycline,but because it depressed ERK /P38MAPK pathways and down-regulated the expression of P-ERK1/2,P-P38 protein.
Publication Year: 2009
Publication Date: 2009-01-01
Language: en
Type: article
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