Document Detail


Cytoprotective effects of albumin, nitrosated or reduced, in cultured rat pulmonary vascular cells.
MedLine Citation:
PMID:  21239532     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
S-nitrosoalbumin (SNO-Alb) has been shown to be an efficacious cytoprotective molecule in acute lung injury, as well as ischemia-reperfusion injury in heart and skeletal muscle. Nonetheless, limited information is available on the cellular mechanism of such protection. Accordingly, we investigated the protective effects of SNO-Alb [ and its denitrosated congener, reduced albumin (SH-Alb) ] on tert-butyl hydroperoxide (tBH)-mediated cytotoxicity in cultured rat pulmonary microvascular endothelial cells (RPMEC), as well as hydrogen sulfide (H(2)S)-mediated cytotoxicity in rat pulmonary artery smooth muscle cells (RPASMC). We noted that tBH caused a concentration-dependent necrosis in RPMEC, and pretreatment of RPMEC with SNO-Alb dose-dependently decreased the sensitivity of these cells to tBH. A component of SNO-Alb cytoprotection was sensitive to N(G)-nitro-L-arginine methyl ester and was associated with activation of endothelial nitric oxide synthase (eNOS), phenomena that could be reproduced with pretreatment with SH-Alb. Exogenous H(2)S caused concentration-dependent apoptosis in RPASMC due to activation of ERK1/2 and p38, as well as downregulation of Bcl-2. Pretreatment with SNO-Alb reduced H(2)S-mediated apoptosis in a concentration-dependent manner that was associated with SNO-Alb-mediated inhibition of activation of ERK1/2 and p38. Pretreatment with SNO-Alb reduced toxicity of 1 mM sodium hydrosulfide in an N(G)-nitro-L-arginine methyl ester-sensitive fashion in RPASMC that expressed gp60 and neuronal NOS and was capable of transporting fluorescently labeled SH-Alb. Therefore, SNO-Alb is cytoprotective against models of oxidant-induced necrosis (tBH) and inhibitors of cellular respiration and apoptosis (H(2)S) in both pulmonary endothelium and smooth muscle, respectively, and a component of such protection can be attributed to a SH-Alb-mediated activation of constitutive NOS.
Authors:
Hui-Hua Li; Jing Xu; Karla J Wasserloos; Jin Li; Yulia Y Tyurina; Valerian E Kagan; Xiaorong Wang; Alex F Chen; Zhao-Qian Liu; Detcho Stoyanovsky; Bruce R Pitt; Li-Ming Zhang
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-01-14
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  300     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-31     Completed Date:  2011-09-15     Revised Date:  2012-04-02    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L526-33     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects
Arteries / cytology
Cells, Cultured
Cytoprotection / drug effects*
Endocytosis / drug effects
Endothelial Cells / cytology*,  drug effects*,  enzymology
Humans
Hydrogen Sulfide / pharmacology
Lung / blood supply*
Microvessels / cytology
Myocytes, Smooth Muscle / cytology,  drug effects
Necrosis / pathology
Nitric Oxide Synthase Type III / metabolism
Nitrosation / drug effects
Nitroso Compounds / pharmacology*
Oxidation-Reduction / drug effects
Rats
Serum Albumin, Bovine / pharmacology*
tert-Butylhydroperoxide / pharmacology
Grant Support
ID/Acronym/Agency:
HL-094488/HL/NHLBI NIH HHS; HL-70755/HL/NHLBI NIH HHS; K08 HL79456-01A1/HL/NHLBI NIH HHS; P50 GM53789/GM/NIGMS NIH HHS; R37 HL65697/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Nitroso Compounds; 0/S-nitrosoalbumin; 0/Serum Albumin, Bovine; 75-91-2/tert-Butylhydroperoxide; 7783-06-4/Hydrogen Sulfide; EC 1.14.13.39/Nitric Oxide Synthase Type III

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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