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Article: Cell cycle-dependent expression of potassium channels and cell proliferation in rat mesenchymal stem cells from bone marrow

TitleCell cycle-dependent expression of potassium channels and cell proliferation in rat mesenchymal stem cells from bone marrow
Authors
Issue Date2007
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CPR
Citation
Cell Proliferation, 2007, v. 40 n. 5, p. 656-670 How to Cite?
AbstractObjective: Recently, our team has demonstrated that voltage-gated delayed rectifier K+ current (IKDR) and Ca2+-activated K+ current (IKCa) are present in rat bone marrow-derived mesenchymal stem cells; however, little is known of their physiological roles. The present study was designed to investigate whether functional expression of IKDR and IKCa would change with cell cycle progression, and whether they could regulate proliferation in undifferentiated rat mesenchymal stem cells (MSCs). Materials and Methods: Membrane potentials and ionic currents were recorded using whole-cell patch clamp technique, cell cycling was analysed by flow cytometry, cell proliferation was assayed with DNA incorporation method and the related genes were down-regulated by RNA interference (RNAi) and examined using RT-PCR. Results: It was found that membrane potential hyperpolarized, and cell size increased during the cell cycle. In addition, IKDR decreased, while IKCa increased during progress from G1 to S phase. RT-PCR revealed that the mRNA levels of Kv1.2 and Kv2.1 (likely responsible for IKDR) reduced, whereas the mRNA level of KCa3.1 (responsible for intermediate-conductance IKCa) increased with the cell cycle progression. Down-regulation of Kv1.2, Kv2.1 or KCa3.1 with the specific RNAi, targeted to corresponding gene inhibited proliferation of rat MSCs. Conclusion: These results demonstrate that membrane potential, IKDR and IKCa channels change with cell cycle progression and corresponding alteration of gene expression. IK DR and intermediate-conductance IKCa play an important role in maintaining membrane potential and they participate in modulation of proliferation in rat MSCs. © 2007 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/77372
ISSN
2015 Impact Factor: 3.084
2015 SCImago Journal Rankings: 1.176
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDeng, XLen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorLai, Ken_HK
dc.contributor.authorCheung, KFen_HK
dc.contributor.authorLau, GKen_HK
dc.contributor.authorLi, GRen_HK
dc.date.accessioned2010-09-06T07:31:11Z-
dc.date.available2010-09-06T07:31:11Z-
dc.date.issued2007en_HK
dc.identifier.citationCell Proliferation, 2007, v. 40 n. 5, p. 656-670en_HK
dc.identifier.issn0960-7722en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77372-
dc.description.abstractObjective: Recently, our team has demonstrated that voltage-gated delayed rectifier K+ current (IKDR) and Ca2+-activated K+ current (IKCa) are present in rat bone marrow-derived mesenchymal stem cells; however, little is known of their physiological roles. The present study was designed to investigate whether functional expression of IKDR and IKCa would change with cell cycle progression, and whether they could regulate proliferation in undifferentiated rat mesenchymal stem cells (MSCs). Materials and Methods: Membrane potentials and ionic currents were recorded using whole-cell patch clamp technique, cell cycling was analysed by flow cytometry, cell proliferation was assayed with DNA incorporation method and the related genes were down-regulated by RNA interference (RNAi) and examined using RT-PCR. Results: It was found that membrane potential hyperpolarized, and cell size increased during the cell cycle. In addition, IKDR decreased, while IKCa increased during progress from G1 to S phase. RT-PCR revealed that the mRNA levels of Kv1.2 and Kv2.1 (likely responsible for IKDR) reduced, whereas the mRNA level of KCa3.1 (responsible for intermediate-conductance IKCa) increased with the cell cycle progression. Down-regulation of Kv1.2, Kv2.1 or KCa3.1 with the specific RNAi, targeted to corresponding gene inhibited proliferation of rat MSCs. Conclusion: These results demonstrate that membrane potential, IKDR and IKCa channels change with cell cycle progression and corresponding alteration of gene expression. IK DR and intermediate-conductance IKCa play an important role in maintaining membrane potential and they participate in modulation of proliferation in rat MSCs. © 2007 The Authors.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CPRen_HK
dc.relation.ispartofCell Proliferationen_HK
dc.rightsCell Proliferation. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshBone Marrow Cells - cytology - metabolismen_HK
dc.subject.meshCell Cycleen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCell Sizeen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshDNA Primers - geneticsen_HK
dc.subject.meshMembrane Potentialsen_HK
dc.subject.meshMesenchymal Stem Cells - cytology - metabolismen_HK
dc.subject.meshPotassium Channel Blockers - pharmacologyen_HK
dc.subject.meshPotassium Channels - genetics - metabolismen_HK
dc.subject.meshRNA Interferenceen_HK
dc.subject.meshRNA, Messenger - genetics - metabolismen_HK
dc.subject.meshRNA, Small Interfering - geneticsen_HK
dc.subject.meshRatsen_HK
dc.titleCell cycle-dependent expression of potassium channels and cell proliferation in rat mesenchymal stem cells from bone marrowen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0960-7722&volume=40&issue=5&spage=656&epage=670&date=2007&atitle=Cell+cycle-dependent+expression+of+potassium+channels+and+cell+proliferation+in+rat+mesenchymal+stem+cells+from+bone+marrow.++++en_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2184.2007.00458.xen_HK
dc.identifier.pmid17877608-
dc.identifier.scopuseid_2-s2.0-34548689850en_HK
dc.identifier.hkuros139376en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548689850&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume40en_HK
dc.identifier.issue5en_HK
dc.identifier.spage656en_HK
dc.identifier.epage670en_HK
dc.identifier.isiWOS:000249484200003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridDeng, XL=14057894600en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridLai, K=7402135541en_HK
dc.identifier.scopusauthoridCheung, KF=8763216400en_HK
dc.identifier.scopusauthoridLau, GK=7102301257en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.citeulike1673703-

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