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http://purl.uniprot.org/citations/20621093http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Background

Hypoxic exposure contributes to the phenotypic switching of smooth muscle cells (SMCs), while the mechanisms involved in this process is not yet fully elucidated. Myocardin as a co-actor of serum reaction factor plays a crucial role in differentiation of SMCs. This study was aimed to investigate the role of myocardin in hypoxia-induced phenotypic switching of rat pulmonary arterial SMCs (PASMCs).

Methods

Primary PASMCs were cultured under normoxia and hypoxia (3%O(2), 48 h) respectively, and then the cell proliferation was assessed and the expression of SM22α, osteopontin (contractile and synthetic marker of SMCs, respectively), myocardin and platelet-derived growth factor-BB (PDGF-BB) were detected. After pGCSIL-GFP-shMYOCD lentviral vector was transduced to the PASMCs, the expression of myocardin and SM22α were examined. Moreover, myocardin expression in PASMCs treated with medium enriched with PDGF-BB and conditional medium (CM) from normoxia- and hypoxia-exposed PASMCs was assessed.

Results

Exposing PASMCs to hypoxia led to an increased cell numbers and the up-regulation of proliferating cell nuclear antigen (PCNA), osteopontin and PDGF-BB; moreover, a significant down-regulation of SM22α and myocardin was identified. Further analysis revealed that knock-down of myocardin with pGCSIL-GFP-shMYOCD vector followed by a decreased SM22α in the PASMCs, and treatment of PASMCs with either exogenous PDGF-BB or hypoxic CM led to a marked decrease of myocardin.

Conclusions

Our findings suggest that the decrease of myocardin in PASMCs exposed to hypoxia is partly regulated by the increase of PDGF-BB, which contributes to the phenotypic switching of PASMCs in hypoxic condition."xsd:string
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http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/author"Guo J."xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/author"Wang G."xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/author"Wang X."xsd:string
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http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/author"Zheng S."xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/author"Ao Q."xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/author"Jie W."xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/name"Exp Mol Pathol"xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/pages"301-306"xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/title"Contribution of myocardin in the hypoxia-induced phenotypic switching of rat pulmonary arterial smooth muscle cells."xsd:string
http://purl.uniprot.org/citations/20621093http://purl.uniprot.org/core/volume"89"xsd:string
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