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Article: Insulin-mediated upregulation of KCa3.1 channels promotes cell migration and proliferation in rat vascular smooth muscle

TitleInsulin-mediated upregulation of KCa3.1 channels promotes cell migration and proliferation in rat vascular smooth muscle
Authors
KeywordsERK1/2
Insulin
Intermediate-conductance Ca 2+ activated K + channel
Migration
Proliferation
VSMCs
Issue Date2011
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 2011, v. 51 n. 1, p. 51-57 How to Cite?
AbstractThe detailed molecular mechanisms underlying pathogenesis of various vascular diseases such as atherosclerosis are not fully understood in type-2 diabetes. The present study was designed to investigate whether insulin regulates K Ca3.1 channels and participates in vasculopathy in type-2 diabetes. A rat model with experimental insulin-resistant type-2 diabetes was used for detecting pathological changes in the aorta wall, and cultured vascular smooth muscle cells (VSMCs) were employed to investigate the regulation of K Ca3.1 channels by insulin and roles of K Ca3.1 channels in cell migration and proliferation using molecular biology and electrophysiology. Early pathological changes were observed and expression of K Ca3.1 channels increased in the aorta wall of the type 2 diabetic rats. K Ca3.1 channel mRNA, protein levels and current density were greatly enhanced in cultured VSMCs treated with insulin, and the effects were countered in the cells treated with the ERK1/2 inhibitor PD98059, but not the p38-MAPK inhibitor SB203580. In addition, insulin stimulated cell migration and proliferation in cultured VSMCs, and the effects were fully reversed in the cells treated with the K Ca3.1 blocker TRAM-34 or PD98059, but not SB203580. These results demonstrate the novel information that insulin increases expression of K Ca3.1 channels by stimulating ERK1/2 phosphorylation thereby promoting migration and proliferation of VSMCs, which likely play at least a partial role in the development of vasculopathy in type-2 diabetes. © 2011 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/133321
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID
Funding AgencyGrant Number
National Nature Science Foundation of China81070129
Doctor Science Foundation of China200806980032
Funding Information:

This work was supported by the National Nature Science Foundation of China (grant number 81070129) and the Doctor Science Foundation of China (grant number 200806980032).

References

 

DC FieldValueLanguage
dc.contributor.authorSu, XLen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorZhang, Wen_HK
dc.contributor.authorZhao, LMen_HK
dc.contributor.authorLi, GRen_HK
dc.contributor.authorDeng, XLen_HK
dc.date.accessioned2011-05-11T08:31:04Z-
dc.date.available2011-05-11T08:31:04Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 2011, v. 51 n. 1, p. 51-57en_HK
dc.identifier.issn0022-2828en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133321-
dc.description.abstractThe detailed molecular mechanisms underlying pathogenesis of various vascular diseases such as atherosclerosis are not fully understood in type-2 diabetes. The present study was designed to investigate whether insulin regulates K Ca3.1 channels and participates in vasculopathy in type-2 diabetes. A rat model with experimental insulin-resistant type-2 diabetes was used for detecting pathological changes in the aorta wall, and cultured vascular smooth muscle cells (VSMCs) were employed to investigate the regulation of K Ca3.1 channels by insulin and roles of K Ca3.1 channels in cell migration and proliferation using molecular biology and electrophysiology. Early pathological changes were observed and expression of K Ca3.1 channels increased in the aorta wall of the type 2 diabetic rats. K Ca3.1 channel mRNA, protein levels and current density were greatly enhanced in cultured VSMCs treated with insulin, and the effects were countered in the cells treated with the ERK1/2 inhibitor PD98059, but not the p38-MAPK inhibitor SB203580. In addition, insulin stimulated cell migration and proliferation in cultured VSMCs, and the effects were fully reversed in the cells treated with the K Ca3.1 blocker TRAM-34 or PD98059, but not SB203580. These results demonstrate the novel information that insulin increases expression of K Ca3.1 channels by stimulating ERK1/2 phosphorylation thereby promoting migration and proliferation of VSMCs, which likely play at least a partial role in the development of vasculopathy in type-2 diabetes. © 2011 Elsevier Ltd.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_HK
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_HK
dc.subjectERK1/2en_HK
dc.subjectInsulinen_HK
dc.subjectIntermediate-conductance Ca 2+ activated K + channelen_HK
dc.subjectMigrationen_HK
dc.subjectProliferationen_HK
dc.subjectVSMCsen_HK
dc.titleInsulin-mediated upregulation of KCa3.1 channels promotes cell migration and proliferation in rat vascular smooth muscleen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2828&volume=51&issue=1&spage=51&epage=57&date=2011&atitle=Insulin-mediated+upregulation+of+K(Ca)3.1+channels+promotes+cell+migration+and+proliferation+in+rat+vascular+smooth+muscle-
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yjmcc.2011.03.014en_HK
dc.identifier.pmid21463632-
dc.identifier.scopuseid_2-s2.0-79956320554en_HK
dc.identifier.hkuros185043en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79956320554&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume51en_HK
dc.identifier.issue1en_HK
dc.identifier.spage51en_HK
dc.identifier.epage57en_HK
dc.identifier.isiWOS:000291580200007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridSu, XL=36446933500en_HK
dc.identifier.scopusauthoridWang, Y=16044156100en_HK
dc.identifier.scopusauthoridZhang, W=36066941200en_HK
dc.identifier.scopusauthoridZhao, LM=37103218900en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.scopusauthoridDeng, XL=14057894600en_HK
dc.identifier.citeulike9154973-

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