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Title: Hydrogen sulphide suppresses human atrial fibroblast proliferation and transformation to myofibroblasts
Authors: Sheng, J
Shim, W 
Wei, H 
Lim, S.Y
Liew, R 
Lim, T.S
Ong, B.H
Chua, Y.L 
Wong, P
Keywords: hydrogen sulfide
potassium channel
primer DNA
atrial fibrosis
cell differentiation
drug effect
heart atrium
nucleotide sequence
polymerase chain reaction
atrial fibrosis
hydrogen sulphide
potassium channel
Base Sequence
Cell Differentiation
DNA Primers
Heart Atria
Hydrogen Sulfide
Polymerase Chain Reaction
Issue Date: 2013
Citation: Sheng, J, Shim, W, Wei, H, Lim, S.Y, Liew, R, Lim, T.S, Ong, B.H, Chua, Y.L, Wong, P (2013). Hydrogen sulphide suppresses human atrial fibroblast proliferation and transformation to myofibroblasts. Journal of Cellular and Molecular Medicine 17 (10) : 1345-1354. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Cardiac fibroblasts are crucial in pathophysiology of the myocardium whereby their aberrant proliferation has significant impact on cardiac function. Hydrogen sulphide (H2S) is a gaseous modulator of potassium channels on cardiomyocytes and has been reported to attenuate cardiac fibrosis. Yet, the mechanism of H2S in modulating proliferation of cardiac fibroblasts remains poorly understood. We hypothesized that H2S inhibits proliferative response of atrial fibroblasts through modulation of potassium channels. Biophysical property of potassium channels in human atrial fibroblasts was examined by whole-cell patch clamp technique and their cellular proliferation in response to H2S was assessed by BrdU assay. Large conductance Ca2+-activated K+ current (BKCa), transient outward K+ current (Ito) and inwardly rectifying K+ current (IKir) were found in human atrial fibroblasts. Current density of BKCa (IC50 = 69.4 μM; n = 6), Ito (IC50 = 55.1 μM; n = 6) and IKir (IC50 = 78.9 μM; n = 6) was significantly decreased (P < 0.05) by acute exposure to NaHS (a H2S donor) in atrial fibroblasts. Furthermore, NaHS (100-500 μM) inhibited fibroblast proliferation induced by transforming growth factor-β1 (TGF-β1; 1 ng/ml), Ang II (100 nM) or 20% FBS. Pre-conditioning of fibroblasts with NaHS decreased basal expression of Kv4.3 (encode Ito), but not KCa1.1 (encode BKCa) and Kir2.1 (encode IKir). Furthermore, H2S significantly attenuated TGF-β1-stimulated Kv4.3 and α-smooth muscle actin expression, which coincided with its inhibition of TGF-β-induced myofibroblast transformation. Our results show that H2S attenuates atrial fibroblast proliferation via suppression of K+ channel activity and moderates their differentiation towards myofibroblasts. © 2013 The Authors.
Source Title: Journal of Cellular and Molecular Medicine
ISSN: 15821838
DOI: 10.1111/jcmm.12114
Rights: Attribution 4.0 International
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