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Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells.
Pharmacol Res. 2010 Apr; 61(4):298-305.PR

Abstract

We previously reported that the endogenous cystathionine gamma-lyase (CSE)/hydrogen sulfide (H(2)S) pathway is implicated in the pathogenesis of bleomycin-induced pulmonary fibrosis in rats, but the exact cellular mechanisms are not well characterized. Epithelial-mesenchymal transition (EMT), induced by transforming growth factor beta1 (TGF-beta1) in alveolar epithelial cells, plays an important role in the pathogenesis of pulmonary fibrosis. We studied whether H(2)S could attenuate EMT in cultured alveolar epithelial cells and TGF-beta1 treatment suppressed CSE expression in A549 cells. Inhibition of endogenous CSE by dl-propargylglycine led to spontaneous EMT, as manifested by decreased E-cadherin level, increased vimentin expression and fibroblast-like morphologic features. Exogenous H(2)S applied to TGF-beta1-treated A549 cells decreased vimentin expression, increased E-cadherin level and retained epithelial morphologic features. In addition, preincubation with H(2)S decreased Smad2/3 phosphorylation in A549 cells stimulated by TGF-beta1, and H(2)S-inhibited alveolar EMT was mimicked by treatment with SB505124, a Smad2/3 inhibitor, but not pinacidil, an ATP-sensitive K(+) channel (K(ATP)) opener. H(2)S serves a critical role in preserving an epithelial phenotype and in attenuating EMT in alveolar epithelial cells, mediated, at least in part, by decreased Smad2/3 phosphorylation and not dependent on K(ATP) channel opening.

Authors+Show Affiliations

Department of Geriatrics, Peking University First Hospital, Xishiku Street No. 8, West District, Beijing, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19913099

Citation

Fang, Li-Ping, et al. "Hydrogen Sulfide Attenuates Epithelial-mesenchymal Transition of Human Alveolar Epithelial Cells." Pharmacological Research, vol. 61, no. 4, 2010, pp. 298-305.
Fang LP, Lin Q, Tang CS, et al. Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells. Pharmacol Res. 2010;61(4):298-305.
Fang, L. P., Lin, Q., Tang, C. S., & Liu, X. M. (2010). Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells. Pharmacological Research, 61(4), 298-305. https://doi.org/10.1016/j.phrs.2009.10.008
Fang LP, et al. Hydrogen Sulfide Attenuates Epithelial-mesenchymal Transition of Human Alveolar Epithelial Cells. Pharmacol Res. 2010;61(4):298-305. PubMed PMID: 19913099.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells. AU - Fang,Li-Ping, AU - Lin,Qing, AU - Tang,Chao-Shu, AU - Liu,Xin-Min, Y1 - 2009/11/11/ PY - 2009/07/13/received PY - 2009/10/25/revised PY - 2009/10/28/accepted PY - 2009/11/17/entrez PY - 2009/11/17/pubmed PY - 2010/6/18/medline SP - 298 EP - 305 JF - Pharmacological research JO - Pharmacol Res VL - 61 IS - 4 N2 - We previously reported that the endogenous cystathionine gamma-lyase (CSE)/hydrogen sulfide (H(2)S) pathway is implicated in the pathogenesis of bleomycin-induced pulmonary fibrosis in rats, but the exact cellular mechanisms are not well characterized. Epithelial-mesenchymal transition (EMT), induced by transforming growth factor beta1 (TGF-beta1) in alveolar epithelial cells, plays an important role in the pathogenesis of pulmonary fibrosis. We studied whether H(2)S could attenuate EMT in cultured alveolar epithelial cells and TGF-beta1 treatment suppressed CSE expression in A549 cells. Inhibition of endogenous CSE by dl-propargylglycine led to spontaneous EMT, as manifested by decreased E-cadherin level, increased vimentin expression and fibroblast-like morphologic features. Exogenous H(2)S applied to TGF-beta1-treated A549 cells decreased vimentin expression, increased E-cadherin level and retained epithelial morphologic features. In addition, preincubation with H(2)S decreased Smad2/3 phosphorylation in A549 cells stimulated by TGF-beta1, and H(2)S-inhibited alveolar EMT was mimicked by treatment with SB505124, a Smad2/3 inhibitor, but not pinacidil, an ATP-sensitive K(+) channel (K(ATP)) opener. H(2)S serves a critical role in preserving an epithelial phenotype and in attenuating EMT in alveolar epithelial cells, mediated, at least in part, by decreased Smad2/3 phosphorylation and not dependent on K(ATP) channel opening. SN - 1096-1186 UR - https://www.unboundmedicine.com/medline/citation/19913099/Hydrogen_sulfide_attenuates_epithelial_mesenchymal_transition_of_human_alveolar_epithelial_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1043-6618(09)00269-2 DB - PRIME DP - Unbound Medicine ER -