Document Detail


Hydrogen sulfide induces apoptosis of pulmonary artery smooth muscle cell in rats with pulmonary hypertension induced by high pulmonary blood flow.
MedLine Citation:
PMID:  20137497     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Abnormal apoptosis of pulmonary artery smooth muscle cells (PASMCs) is an important pathophysiological process in the pulmonary artery structural remodeling and pulmonary hypertension. We investigated possible effect of endogenous hydrogen sulfide (H2S) on apoptosis of PASMCs during the development of pulmonary hypertension induced by high pulmonary blood flow. METHODS: Thirty-nine male Sprague-Dawley rats were randomly assigned to 4-week control, 4-week shunt, 4-week shunt + propargylglycine (PPG), 11-week control, 11-week shunt and 11-week shunt + sodium hydrosulfide (NaHS) groups. Rats in 4-week shunt, 4-week shunt + PPG, 11-week shunt and 11-week shunt + NaHS groups underwent an abdominal aorta-inferior vena cava shunt. Rats in 4-week shunt + PPG group were intraperitoneally injected with PPG, an inhibitor of endogenous H2S production, for 4 weeks. Rats in 11-week shunt + NaHS group were intraperitoneally injected with NaHS, a H2S donor, for 11 weeks. Lung tissue H2S was evaluated by sulfide-sensitive electrode. Apoptosis of PASMCs were detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL). Expressions of Fas, bcl-2 and caspase-3 in the PASMCs were analyzed with immunochemical staining. RESULTS: Four weeks after the shunting operation, the apoptosis of PASMCs and expression of Fas and caspase-3 were significantly decreased (P < 0.01), but expression of bcl-2 increased significantly (P < 0.01). PPG administration further inhibited the apoptosis of PASMCs, downregulated the expression of Fas and caspase-3 (P < 0.01), but increased the expression of bcl-2 (P < 0.01). After 11 weeks of shunting operation, the apoptosis of PASMCs and expression of Fas and caspase-3 were significantly decreased (P < 0.01), but expression of bcl-2 increased obviously (P < 0.01). NaHS administration significantly increased the apoptosis of PASMCs, upregulated the expression of Fas and caspase-3, but inhibited the expression of bcl-2. CONCLUSIONS: H2S induces the apoptosis of PASMCs in the development of high pulmonary blood flow-induced pulmonary hypertension by activating the Fas pathway and inhibiting the bcl-2 pathway.
Authors:
Wei Li; Hong-Fang Jin; Die Liu; Jing-Hui Sun; Pei-Jun Jian; Xiao-Hui Li; Chao-Shu Tang; Jun-Bao DU
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Chinese medical journal     Volume:  122     ISSN:  0366-6999     ISO Abbreviation:  Chin. Med. J.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2010-02-08     Completed Date:  2010-04-30     Revised Date:  2010-09-14    
Medline Journal Info:
Nlm Unique ID:  7513795     Medline TA:  Chin Med J (Engl)     Country:  China    
Other Details:
Languages:  eng     Pagination:  3032-8     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
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MeSH Terms
Descriptor/Qualifier:
Alkynes / pharmacology
Animals
Apoptosis / drug effects*
Blood Flow Velocity / physiology
Blotting, Western
Glycine / analogs & derivatives,  pharmacology
Hemodynamics / drug effects
Hydrogen Sulfide / pharmacology*
Hypertension, Pulmonary / etiology*,  physiopathology*
Immunohistochemistry
In Situ Nick-End Labeling
Male
Myocytes, Smooth Muscle / cytology*,  drug effects*
Pulmonary Artery / cytology*
Random Allocation
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Alkynes; 56-40-6/Glycine; 64165-64-6/propargylglycine; 7783-06-4/Hydrogen Sulfide

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