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Article: Regulation of cell proliferation by intermediate-conductance Ca 2+-activated potassium and volume-sensitive chloride channels in mouse mesenchymal stem cells

TitleRegulation of cell proliferation by intermediate-conductance Ca 2+-activated potassium and volume-sensitive chloride channels in mouse mesenchymal stem cells
Authors
Issue Date2008
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 2008, v. 295 n. 5, p. C1409-C1416 How to Cite?
AbstractBone marrow mesenchymal stem cells (MSCs) are a promising cell source for regenerative medicine; however, their cellular physiology is not fully understood. The present study aimed at exploring the potential roles of the two dominant functional ion channels, intermediate-conductance Ca 2+-activated potassium (IKCa) and volume-sensitive chloride (ICl.vol) channels, in regulating proliferation of mouse MSCs. We found that inhibition of IKCa with clotrimazole and I Cl.vol with 5-nitro-1-(3-phenylpropylamino) benzoic acid (NPPB) reduced cell proliferation in a concentration-dependent manner. Knockdown of KCa3.1 or Clcn3 with specific short interference (si)RNAs significantly reduced IKCa or ICl.vol density and channel protein and produced a remarkable suppression of cell proliferation (by 24.4 ± 9.6% and 29.5 ± 7.2%, respectively, P < 0.05 vs. controls). Flow cytometry analysis showed that mouse MSCs retained at G0/G1 phase (control: 51.65 ± 3.43%) by inhibiting IKCa or ICl.vol using clotrimazole (2 μM: 64.45 ± 2.20%, P < 0.05) or NPPB (200 μM: 82.89 ± 2.49%, P < 0.05) or the specific siRNAs, meanwhile distribution of cells in S phase was decreased. Western blot analysis revealed a reduced expression of the cell cycle regulatory proteins cyclin D1 and cyclin E. Collectively, our results have demonstrated that IKCa and I Cl.vol channels regulate cell cycle progression and proliferation of mouse MSCs by modulating cyclin D1 and cyclin E expression. Copyright © 2008 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/163217
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTao, Ren_US
dc.contributor.authorLau, CPen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorLi, GRen_US
dc.date.accessioned2012-09-05T05:28:49Z-
dc.date.available2012-09-05T05:28:49Z-
dc.date.issued2008en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2008, v. 295 n. 5, p. C1409-C1416en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/163217-
dc.description.abstractBone marrow mesenchymal stem cells (MSCs) are a promising cell source for regenerative medicine; however, their cellular physiology is not fully understood. The present study aimed at exploring the potential roles of the two dominant functional ion channels, intermediate-conductance Ca 2+-activated potassium (IKCa) and volume-sensitive chloride (ICl.vol) channels, in regulating proliferation of mouse MSCs. We found that inhibition of IKCa with clotrimazole and I Cl.vol with 5-nitro-1-(3-phenylpropylamino) benzoic acid (NPPB) reduced cell proliferation in a concentration-dependent manner. Knockdown of KCa3.1 or Clcn3 with specific short interference (si)RNAs significantly reduced IKCa or ICl.vol density and channel protein and produced a remarkable suppression of cell proliferation (by 24.4 ± 9.6% and 29.5 ± 7.2%, respectively, P < 0.05 vs. controls). Flow cytometry analysis showed that mouse MSCs retained at G0/G1 phase (control: 51.65 ± 3.43%) by inhibiting IKCa or ICl.vol using clotrimazole (2 μM: 64.45 ± 2.20%, P < 0.05) or NPPB (200 μM: 82.89 ± 2.49%, P < 0.05) or the specific siRNAs, meanwhile distribution of cells in S phase was decreased. Western blot analysis revealed a reduced expression of the cell cycle regulatory proteins cyclin D1 and cyclin E. Collectively, our results have demonstrated that IKCa and I Cl.vol channels regulate cell cycle progression and proliferation of mouse MSCs by modulating cyclin D1 and cyclin E expression. Copyright © 2008 the American Physiological Society.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Cycle - Drug Effectsen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshCell Sizeen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChloride Channels - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshClotrimazole - Pharmacologyen_US
dc.subject.meshCyclin D1 - Metabolismen_US
dc.subject.meshCyclin E - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshIntermediate-Conductance Calcium-Activated Potassium Channels - Antagonists & Inhibitors - Genetics - Metabolismen_US
dc.subject.meshMembrane Potentialsen_US
dc.subject.meshMesenchymal Stem Cells - Drug Effects - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshNitrobenzoates - Pharmacologyen_US
dc.subject.meshPotassium Channel Blockers - Pharmacologyen_US
dc.subject.meshRna Interferenceen_US
dc.subject.meshRna, Small Interfering - Metabolismen_US
dc.titleRegulation of cell proliferation by intermediate-conductance Ca 2+-activated potassium and volume-sensitive chloride channels in mouse mesenchymal stem cellsen_US
dc.typeArticleen_US
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1152/ajpcell.00268.2008en_US
dc.identifier.pmid18815226-
dc.identifier.scopuseid_2-s2.0-57349113856en_US
dc.identifier.hkuros152676-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-57349113856&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume295en_US
dc.identifier.issue5en_US
dc.identifier.spageC1409en_US
dc.identifier.epageC1416en_US
dc.identifier.isiWOS:000262909800035-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTao, R=7102857104en_US
dc.identifier.scopusauthoridLau, CP=7401968501en_US
dc.identifier.scopusauthoridTse, HF=7006070805en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US

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