Effects of endogenous carbon monoxide on gene expression profiles associated with the apoptosis of pulmonary arterial smooth muscle cells.
- Author:
Xiao-Jie SUN
1
;
Li YU
;
Xiao-Qin WANG
;
Zhong-Qiang LIU
;
Juan WANG
;
Zheng-Xiang GAO
;
Han-Min LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Carbon Monoxide; physiology; Gene Expression Profiling; Hemin; pharmacology; Male; Muscle, Smooth, Vascular; pathology; Myocytes, Smooth Muscle; pathology; Pulmonary Artery; pathology; Rats; Rats, Sprague-Dawley; Signal Transduction; Tumor Suppressor Protein p53; physiology; p38 Mitogen-Activated Protein Kinases; physiology
- From: Chinese Journal of Contemporary Pediatrics 2010;12(11):882-885
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo identify the gene expression profiles associated with the apoptosis of pulmonary arterial smooth muscle cells stimulated by carbon monoxide (CO).
METHODSPrimary cultured Sprague-Dawley rat pulmonary arterial smooth muscle cells (PASMC) were stimulated by platelet-derived growth factor (PDGF, 20 ng/mL) and hemin (20 μmol/L). Cells were harvested after 2 hrs and Affymetrix microarrays were used to detect the gene expression profile.
RESULTSSome genes associated with Map2k3 (P38) signal pathway, such as CyclinD1, CyclinH, CyclinL1, MAP2K3, Kras and Nras, were upregulated, but P27 expression was downregulated after PDGF treatment. After endogenous CO treatment, some genes associated with P53 pathway, such as Gadd45α, P21 and Trp53inp1, were upregulated.
CONCLUSIONSP53 pathway probably plays an important role in apoptosis of pulmonary arterial smooth muscle cells treated with endogenous CO.
