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Article: Multiple Ca2+ signaling pathways regulate intracellular Ca 2+ activity in human cardiac fibroblasts

TitleMultiple Ca2+ signaling pathways regulate intracellular Ca 2+ activity in human cardiac fibroblasts
Authors
Issue Date2010
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010
Citation
Journal Of Cellular Physiology, 2010, v. 223 n. 1, p. 68-75 How to Cite?
AbstractCa2+ signaling pathways are well studied in cardiac myocytes, but not in cardiac fibroblasts. The aim of the present study is to characterize Ca2+ signaling pathways in cultured human cardiac fibroblasts using confocal scanning microscope and RT-PCR techniques. It was found that spontaneous intracellular Ca2+ (Cai 2+) oscillations were present in about 29% of human cardiac fibroblasts, and the number of cells with Cai 2+ oscillations was increased to 57.3% by application of 3% fetal bovine serum. Cai 2+ oscillations were dependent on Ca2+ entry. Cai2+ oscillations were abolished by the store-operated Ca2+ (SOC) entry channel blocker La3+, the phospholipase C inhibitor U-73122, and the inositol trisphosphate receptors (IP3Rs) inhibitor 2-aminoethoxydiphenyl borate, but not by ryanodine. The IP3R agonist thimerosal enhanced Ca2+ i oscillations. Inhibition of plasma membrane Ca2+ pump (PMCA) and Na+-Ca2+ exchanger (NCX) also suppressed Ca i 2+ oscillations. In addition, the frequency of Ca i 2+ oscillations was reduced by nifedipine, and increased by Bay K8644 in cells with spontaneous Cai 2+ oscillations. RT-PCR revealed that mRNAs for IP3R1-3, SERCA1-3, CaV1.2, NCX3, PMCA1,3,4, TRPC1,3,4,6, STIM1, and Orai1-3, were readily detectable, but not RyRs. Our results demonstrate for the first time that spontaneous Cai 2+ oscillations are present in cultured human cardiac fibroblasts and are regulated by multiple Ca2+ pathways, which are not identical to those of the well-studied contractile cardiomyocytes. This study provides a base for future investigations into how Ca2+ signals regulate biological activity in human cardiac fibroblasts and cardiac remodeling under pathological conditions. © 2009 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/77685
ISSN
2015 Impact Factor: 4.155
2015 SCImago Journal Rankings: 1.842
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council of Hong KongHKU 760306M
HKU 770108M
Funding Information:

Contract grant sponsor: General Research Funds (Research Grant Council of Hong Kong);

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorChen, JBen_HK
dc.contributor.authorTao, Ren_HK
dc.contributor.authorSun, HYen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorLi, GRen_HK
dc.date.accessioned2010-09-06T07:34:36Z-
dc.date.available2010-09-06T07:34:36Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Cellular Physiology, 2010, v. 223 n. 1, p. 68-75en_HK
dc.identifier.issn0021-9541en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77685-
dc.description.abstractCa2+ signaling pathways are well studied in cardiac myocytes, but not in cardiac fibroblasts. The aim of the present study is to characterize Ca2+ signaling pathways in cultured human cardiac fibroblasts using confocal scanning microscope and RT-PCR techniques. It was found that spontaneous intracellular Ca2+ (Cai 2+) oscillations were present in about 29% of human cardiac fibroblasts, and the number of cells with Cai 2+ oscillations was increased to 57.3% by application of 3% fetal bovine serum. Cai 2+ oscillations were dependent on Ca2+ entry. Cai2+ oscillations were abolished by the store-operated Ca2+ (SOC) entry channel blocker La3+, the phospholipase C inhibitor U-73122, and the inositol trisphosphate receptors (IP3Rs) inhibitor 2-aminoethoxydiphenyl borate, but not by ryanodine. The IP3R agonist thimerosal enhanced Ca2+ i oscillations. Inhibition of plasma membrane Ca2+ pump (PMCA) and Na+-Ca2+ exchanger (NCX) also suppressed Ca i 2+ oscillations. In addition, the frequency of Ca i 2+ oscillations was reduced by nifedipine, and increased by Bay K8644 in cells with spontaneous Cai 2+ oscillations. RT-PCR revealed that mRNAs for IP3R1-3, SERCA1-3, CaV1.2, NCX3, PMCA1,3,4, TRPC1,3,4,6, STIM1, and Orai1-3, were readily detectable, but not RyRs. Our results demonstrate for the first time that spontaneous Cai 2+ oscillations are present in cultured human cardiac fibroblasts and are regulated by multiple Ca2+ pathways, which are not identical to those of the well-studied contractile cardiomyocytes. This study provides a base for future investigations into how Ca2+ signals regulate biological activity in human cardiac fibroblasts and cardiac remodeling under pathological conditions. © 2009 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010en_HK
dc.relation.ispartofJournal of Cellular Physiologyen_HK
dc.rightsJournal of cellular physiology. Copyright © John Wiley & Sons, Inc.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThis is a preprint of an article published in Journal of cellular physiology, 2010, v. 223 n. 1, p. 68-75-
dc.subject.meshCalcium - metabolism-
dc.subject.meshCalcium Signaling - drug effects - genetics-
dc.subject.meshEnzyme Inhibitors - pharmacology-
dc.subject.meshFibroblasts - drug effects - metabolism-
dc.subject.meshHeart Ventricles - cytology - drug effects - metabolism-
dc.titleMultiple Ca2+ signaling pathways regulate intracellular Ca 2+ activity in human cardiac fibroblastsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9541&volume=223&issue=1&spage=68&epage=75&date=2010&atitle=Multiple+Ca(2+)+signaling+pathways+regulate+intracellular+Ca(2+)+activity+in+human+cardiac+fibroblastsen_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1002/jcp.22010en_HK
dc.identifier.pmid20039269-
dc.identifier.scopuseid_2-s2.0-75749134126en_HK
dc.identifier.hkuros168452en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-75749134126&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume223en_HK
dc.identifier.issue1en_HK
dc.identifier.spage68en_HK
dc.identifier.epage75en_HK
dc.identifier.isiWOS:000275589300008-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectCalcium Signals and Cell Proliferation in Human Cardiac Fibroblasts-
dc.identifier.scopusauthoridChen, JB=35213097600en_HK
dc.identifier.scopusauthoridTao, R=7102857104en_HK
dc.identifier.scopusauthoridSun, HY=35723049200en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK

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