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Conference Paper: Large-conductance Ca(2+)-activated potassium and ether-a-go-go potassium channels regulate proliferation of human mesenchymal stem cells

TitleLarge-conductance Ca(2+)-activated potassium and ether-a-go-go potassium channels regulate proliferation of human mesenchymal stem cells
Authors
KeywordsCardiovascular disease
Issue Date2009
PublisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
Citation
The 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 59, abstract no. P11 How to Cite?
AbstractBACKGROUND: Bone marrow-derived mesenchymal stem cells (MSCs) are a promising cell source for regenerative medicine; however, cellular physiology is not fully understood in human MSCs. The present study was to explore the potential role of the dominant functional ion channels, large-conductance Ca2+-activated potassium (BKCa) channel, ether-à-go-go potassium (hEAG1) channel, and sodium channel, in regulating proliferation of human MSCs using whole-cell patch clamp and cell proliferation assay approaches. RESULTS: We found that the BKCa channel blocker paxilline (1 μM) almost fully inhibited BKCa current (from 6.76±0.99 pA/pF of control, to 0.02±0.09 pA/pF at +100 mV, n=5, P<0.05) in human MSCs. The hEAG1 channel blocker astemizole (0.5 μM) significantly reduced hEAG1 current from 4.28±1.86 pA/pF to 1.40±1.13 pA/pF at +50 mV, n=6, P<0.05). The MTT experiment showed that paxilline at 0.3, 1.0, and 3.0 μM reduced cell proliferation to 97.2, 84.4, and 48.7% of control, respectively, and astemizole at 0.3, 0.5, and 1 μM decreased cell proliferation to 96.5, 80.5, and 45.8%, respectively. However, the sodium channel blocker tetrodotoxin (1 μM, fully blocked sodium current) had no effect on proliferation in human MSCs. 3H-thymidine incorporation assay demonstrated that both paxilline and astemizole reduced DNA synthesis rate in a concentration-dependent manner. Flowcytometry analysis displayed that inhibition of BKCa channel with 1 μM paxilline or hEAG1 channel with 0.5 μM astemizole accumulated cells at G0/G1 phase (from control 68.9% to 80.5% for paxilline; to 79.2% for astemizole). CONCLUSION: Our results demonstrate that BKCa and hEAG1 channels, but not sodium channel, participate in the regulation of cell proliferation by promoting G0/G1 cells into cell cycling progression.
DescriptionPoster Presentation: abstract no. P11
Persistent Identifierhttp://hdl.handle.net/10722/129836
ISSN
2015 SCImago Journal Rankings: 0.102

 

DC FieldValueLanguage
dc.contributor.authorZhang, YYen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorLau, CPen_US
dc.contributor.authorLi, GRen_US
dc.date.accessioned2010-12-23T08:42:47Z-
dc.date.available2010-12-23T08:42:47Z-
dc.date.issued2009en_US
dc.identifier.citationThe 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 59, abstract no. P11en_US
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/129836-
dc.descriptionPoster Presentation: abstract no. P11-
dc.description.abstractBACKGROUND: Bone marrow-derived mesenchymal stem cells (MSCs) are a promising cell source for regenerative medicine; however, cellular physiology is not fully understood in human MSCs. The present study was to explore the potential role of the dominant functional ion channels, large-conductance Ca2+-activated potassium (BKCa) channel, ether-à-go-go potassium (hEAG1) channel, and sodium channel, in regulating proliferation of human MSCs using whole-cell patch clamp and cell proliferation assay approaches. RESULTS: We found that the BKCa channel blocker paxilline (1 μM) almost fully inhibited BKCa current (from 6.76±0.99 pA/pF of control, to 0.02±0.09 pA/pF at +100 mV, n=5, P<0.05) in human MSCs. The hEAG1 channel blocker astemizole (0.5 μM) significantly reduced hEAG1 current from 4.28±1.86 pA/pF to 1.40±1.13 pA/pF at +50 mV, n=6, P<0.05). The MTT experiment showed that paxilline at 0.3, 1.0, and 3.0 μM reduced cell proliferation to 97.2, 84.4, and 48.7% of control, respectively, and astemizole at 0.3, 0.5, and 1 μM decreased cell proliferation to 96.5, 80.5, and 45.8%, respectively. However, the sodium channel blocker tetrodotoxin (1 μM, fully blocked sodium current) had no effect on proliferation in human MSCs. 3H-thymidine incorporation assay demonstrated that both paxilline and astemizole reduced DNA synthesis rate in a concentration-dependent manner. Flowcytometry analysis displayed that inhibition of BKCa channel with 1 μM paxilline or hEAG1 channel with 0.5 μM astemizole accumulated cells at G0/G1 phase (from control 68.9% to 80.5% for paxilline; to 79.2% for astemizole). CONCLUSION: Our results demonstrate that BKCa and hEAG1 channels, but not sodium channel, participate in the regulation of cell proliferation by promoting G0/G1 cells into cell cycling progression.-
dc.languageengen_US
dc.publisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3-
dc.relation.ispartofJournal of the Hong Kong College of Cardiologyen_US
dc.rightsOpen Access Journal-
dc.subjectCardiovascular disease-
dc.titleLarge-conductance Ca(2+)-activated potassium and ether-a-go-go potassium channels regulate proliferation of human mesenchymal stem cellsen_US
dc.typeConference_Paperen_US
dc.identifier.emailTse, HF: hftse@hku.hken_US
dc.identifier.emailLau, CP: cplau@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_fulltext-
dc.identifier.hkuros177394en_US
dc.identifier.volume17en_US
dc.identifier.issue2en_US
dc.identifier.spage59en_US
dc.identifier.epage59-
dc.publisher.placeHong Kong-
dc.description.otherThe 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 59, abstract no. P11-

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