The effect of carbon monoxide on the proliferation of PASMCs under hypoxia and the mechanism.

Guo-hua Zhen; Zhen-xiang Zhang; Yong-jian XU

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The effect of carbon monoxide on the proliferation of PASMCs under hypoxia and the mechanism.

Author: Guo-Hua ZHEN ¹ ; Zhen-Xiang ZHANG ; Yong-Jian XU
Author Information

1. Department of Respiratory Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Publication Type:Journal Article
MeSH: Animals; Carbon Monoxide; Cell Hypoxia; Cell Proliferation; Cells, Cultured; Muscle, Smooth, Vascular; cytology; metabolism; pathology; Myocytes, Smooth Muscle; cytology; metabolism; Pulmonary Artery; metabolism; Rats; Rats, Wistar
From: Chinese Journal of Applied Physiology 2002;18(3):257-260
CountryChina
Language:Chinese
Abstract:
AIM AND METHODSMTT colorimetric assay, in situ hybridization and immunocytochemistry were performed to investigate the effect of endogenous and exogenous CO on the proliferation of PASMCs and the expression of PDGF-B and protooncogene bcl-2, P53 (mutant type) in PASMCs, in order to elucidate the mechanism by which CO suppressed the proliferation of PASMC in hypoxic environment.
RESULTSThe results of in situ hybridization of PDGF-B mRNA and immunocytochemical staining of PDGF-B were negative. Hypoxia could upregulate the expression of Bcl-2, mutant P53 protein in comparison with the control group (P < 0.01). Compared with the hypoxic group, the expression of Bcl-2 and mutant P53 were decreased after treated with hemin or CO, but increased after treated with hemoglobin (P < 0.01).
CONCLUSIONCO could suppress the expression of oncogene bcl-2 and mutant P53. This partially explained how CO suppressed the proliferation of PASMCs in hypoxic environment.