Methods - We examined the effect of H2S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively.
Results - Exposure of ASM to H2S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous H2S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by H2S donors. Finally, we report that exogenous H2S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells.
Conclusions - H2S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to H2S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for H2S production.
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Data availability statement for 'The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide'.
Perry, M. M. (Creator), Tildy, B. (Creator), Papi, A. (Creator), Casolari, P. (Creator), Caramori, G. (Creator), Rempel, K. L. (Creator), Halayko, A. J. (Creator), Adcock, I. M. (Creator) & Chung, K. F. (Creator), Springer Nature, 9 May 2018
Dataset: Data Availability Statement