Please use this identifier to cite or link to this item: https://doi.org/10.1111/jcmm.12114
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dc.titleHydrogen sulphide suppresses human atrial fibroblast proliferation and transformation to myofibroblasts
dc.contributor.authorSheng, J
dc.contributor.authorShim, W
dc.contributor.authorWei, H
dc.contributor.authorLim, S.Y
dc.contributor.authorLiew, R
dc.contributor.authorLim, T.S
dc.contributor.authorOng, B.H
dc.contributor.authorChua, Y.L
dc.contributor.authorWong, P
dc.date.accessioned2020-10-27T11:17:00Z
dc.date.available2020-10-27T11:17:00Z
dc.date.issued2013
dc.identifier.citationSheng, 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. https://doi.org/10.1111/jcmm.12114
dc.identifier.issn15821838
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/181553
dc.description.abstractCardiac 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.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjecthydrogen sulfide
dc.subjectpotassium channel
dc.subjectprimer DNA
dc.subjectarticle
dc.subjectatrial fibrosis
dc.subjectcell differentiation
dc.subjectcytology
dc.subjectdrug effect
dc.subjectfibroblast
dc.subjectheart atrium
dc.subjecthuman
dc.subjectnucleotide sequence
dc.subjectpolymerase chain reaction
dc.subjectatrial fibrosis
dc.subjectfibroblast
dc.subjecthydrogen sulphide
dc.subjectpotassium channel
dc.subjectBase Sequence
dc.subjectCell Differentiation
dc.subjectDNA Primers
dc.subjectFibroblasts
dc.subjectHeart Atria
dc.subjectHumans
dc.subjectHydrogen Sulfide
dc.subjectPolymerase Chain Reaction
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.contributor.departmentDEPT OF ANATOMY
dc.description.doi10.1111/jcmm.12114
dc.description.sourcetitleJournal of Cellular and Molecular Medicine
dc.description.volume17
dc.description.issue10
dc.description.page1345-1354
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