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Conference Paper: Epidermal Growth Factor Stimulates Cell Proliferation by Activating Voltage-Gated Potassium Channels in Rat Bone Marrow-Derived Mesenchymal Stem Cells

TitleEpidermal Growth Factor Stimulates Cell Proliferation by Activating Voltage-Gated Potassium Channels in Rat Bone Marrow-Derived Mesenchymal Stem Cells
Authors
Issue Date2012
Citation
Hong Kong-Taiwan Physiology Symposium 2012 and Joint Scientific Meeting of Hong Kong Society of Neurosciences (HKSN) & The Biophysical Society of Hong Kong (BPHK), The Chinese University of Hong Kong, Hong Kong, China, 14-15 June 2012, p. 55, abstract no. P20 How to Cite?
AbstractBackground and objective: We have previously found that voltage-gated delayed rectifier potassium current (IKDR, encoded by Kv1.2 and Kv2.1) participated in regulation of cell cycling progression in rat mesenchymal stem cells (MSCs) from bone marrow. The present study was designed to investigate whether epidermal growth factor (EGF) regulates cell growth is mediated by activating IKDR. Methods: Whole-cell patch voltage-clamp, RT-PCR, Western blots, siRNA, cell proliferation assay were employed in the present study Results: EGF increased cell proliferation in a concentration-dependent manner, and the effect was countered by the broad spectrum protein tyrosine (PTK) inhibitor genistein and the EGFR kinase inhibitor AG556. We found that genistein and AG556 inhibited IKDR in a concentration-dependent manner, The protein tyrosine phosphatase (PTP) inhibitor orthovanadate enhanced IKDR, and counted the inhibitory effect of IKDR by genistein or AG556, suggesting the PTK-mediating modulation of IKDR. Interestingly EGF also increased IKDR, Downregulation of IKDR with siRNA targeting to Kv1.2 or Kv2.1 channels inhibited basal proliferation, and prevented EGF-stimulated proliferation in rat MSCs. Conclusion: These results demonstrate for the first time that EGF stimulates cell proliferation activating IKDR, and silencing Kv1.2 or Kv2.1 channels prevents the augmentation of proliferation by EFG, indicating that Kv1.2 and Kv2.1 channels mediate EGF effect in regulating cell growth in rat MSCs.
DescriptionPoster presentation
Persistent Identifierhttp://hdl.handle.net/10722/160310

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_US
dc.contributor.authorDeng, XLen_US
dc.contributor.authorLi, GRen_US
dc.date.accessioned2012-08-16T06:07:56Z-
dc.date.available2012-08-16T06:07:56Z-
dc.date.issued2012en_US
dc.identifier.citationHong Kong-Taiwan Physiology Symposium 2012 and Joint Scientific Meeting of Hong Kong Society of Neurosciences (HKSN) & The Biophysical Society of Hong Kong (BPHK), The Chinese University of Hong Kong, Hong Kong, China, 14-15 June 2012, p. 55, abstract no. P20en_US
dc.identifier.urihttp://hdl.handle.net/10722/160310-
dc.descriptionPoster presentation-
dc.description.abstractBackground and objective: We have previously found that voltage-gated delayed rectifier potassium current (IKDR, encoded by Kv1.2 and Kv2.1) participated in regulation of cell cycling progression in rat mesenchymal stem cells (MSCs) from bone marrow. The present study was designed to investigate whether epidermal growth factor (EGF) regulates cell growth is mediated by activating IKDR. Methods: Whole-cell patch voltage-clamp, RT-PCR, Western blots, siRNA, cell proliferation assay were employed in the present study Results: EGF increased cell proliferation in a concentration-dependent manner, and the effect was countered by the broad spectrum protein tyrosine (PTK) inhibitor genistein and the EGFR kinase inhibitor AG556. We found that genistein and AG556 inhibited IKDR in a concentration-dependent manner, The protein tyrosine phosphatase (PTP) inhibitor orthovanadate enhanced IKDR, and counted the inhibitory effect of IKDR by genistein or AG556, suggesting the PTK-mediating modulation of IKDR. Interestingly EGF also increased IKDR, Downregulation of IKDR with siRNA targeting to Kv1.2 or Kv2.1 channels inhibited basal proliferation, and prevented EGF-stimulated proliferation in rat MSCs. Conclusion: These results demonstrate for the first time that EGF stimulates cell proliferation activating IKDR, and silencing Kv1.2 or Kv2.1 channels prevents the augmentation of proliferation by EFG, indicating that Kv1.2 and Kv2.1 channels mediate EGF effect in regulating cell growth in rat MSCs.-
dc.languageengen_US
dc.relation.ispartofHong Kong-Taiwan Physiology Symposium and Joint Scientific Meeting of Hong Kong Society of Neurosciences & The Biophysical Society of Hong Kongen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleEpidermal Growth Factor Stimulates Cell Proliferation by Activating Voltage-Gated Potassium Channels in Rat Bone Marrow-Derived Mesenchymal Stem Cellsen_US
dc.typeConference_Paperen_US
dc.identifier.emailWang, Y: hannayan@hku.hken_US
dc.identifier.emailLi, GR: grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros202899en_US
dc.identifier.spage55, abstract no. P20en_US
dc.identifier.epage55, abstract no. P20en_US
dc.publisher.placeHong Kong, China-

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