File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: TRPC1 channels mediate the nonselective cation current and store-operated calcium channels in human atrial myocytes

TitleTRPC1 channels mediate the nonselective cation current and store-operated calcium channels in human atrial myocytes
Authors
Issue Date2012
PublisherCell Press. The Journal's web site is located at http://www.cell.com/biophysj/
Citation
The 56th Annual Meeting of Biophysical Society, San Diego, CA., 25-29 February 2012. In Biophysical Journal, 2012, v. 102 n. 3, S1, p. 534a, no. 2719-Pos How to Cite?
AbstractLittle information is available in the literature regarding transient receptor potential (TRP) channels in human atrial myocytes. The present study was designed to investigate whether TRPC channels would mediate the nonselective cation current reported previously and store-operated Ca2+ entry channels (SOCs) in human atrial myocytes using approaches of whole-cell patch voltage-clamp, RT-PCR, Western blot analysis, confocol microscopy, and co-immunoprecipitation. It was found that the nonselective cation current was recorded under K+-free conditions in human atrial myocytes, and the current was inhibited by the nonspecific TRP channel blocker La3+. The TRPC1 channel activator thapsigargin activated the current, and the effect was suppressed by La3+ and prevented by pipette inclusion of anti-TRPC1 antibody. In addition, confocol microscopic experiment revealed intracellular Ca2+ transient mediated by SOCs in human atrial myocytes, which was inhibited or prevented by La3+. The mRNAs and proteins of STIM1 and Orai1 (components of SOCs), were abundantly expressed in human atria. Co-immunoprecipitation analysis demonstrated an interaction of TRPC1 with STIM1 and/or Orai1. Interestingly, protein expression of TRPC1 and STIM1, but not Orai1, was upregulated in human atria with atrial fibrillation. Our results indicate that the novel information that TRPC1 channels not only mediate the nonselective cation current, but also is a component of SOCs in human atria. The upregulation of TRPC1 and STIM1 in human atria with atrial fibrillation may suggest that TRPC1 channels and SOCs are likely involved in the atrial electrical and/or structure remodeling in patients with atrial fibrillation. Copyright © 2011 Biophysical Society. Published by Elsevier Inc. All rights reserved.
DescriptionSession - TRPC Channels, no. 2719-Pos, Board B489
Open Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/146023
ISSN
2015 Impact Factor: 3.632
2015 SCImago Journal Rankings: 2.188

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_US
dc.contributor.authorSun, Hen_US
dc.contributor.authorWu, Hen_US
dc.contributor.authorLi, GRen_US
dc.date.accessioned2012-03-27T09:06:18Z-
dc.date.available2012-03-27T09:06:18Z-
dc.date.issued2012en_US
dc.identifier.citationThe 56th Annual Meeting of Biophysical Society, San Diego, CA., 25-29 February 2012. In Biophysical Journal, 2012, v. 102 n. 3, S1, p. 534a, no. 2719-Posen_US
dc.identifier.issn0006-3495-
dc.identifier.urihttp://hdl.handle.net/10722/146023-
dc.descriptionSession - TRPC Channels, no. 2719-Pos, Board B489-
dc.descriptionOpen Access Journal-
dc.description.abstractLittle information is available in the literature regarding transient receptor potential (TRP) channels in human atrial myocytes. The present study was designed to investigate whether TRPC channels would mediate the nonselective cation current reported previously and store-operated Ca2+ entry channels (SOCs) in human atrial myocytes using approaches of whole-cell patch voltage-clamp, RT-PCR, Western blot analysis, confocol microscopy, and co-immunoprecipitation. It was found that the nonselective cation current was recorded under K+-free conditions in human atrial myocytes, and the current was inhibited by the nonspecific TRP channel blocker La3+. The TRPC1 channel activator thapsigargin activated the current, and the effect was suppressed by La3+ and prevented by pipette inclusion of anti-TRPC1 antibody. In addition, confocol microscopic experiment revealed intracellular Ca2+ transient mediated by SOCs in human atrial myocytes, which was inhibited or prevented by La3+. The mRNAs and proteins of STIM1 and Orai1 (components of SOCs), were abundantly expressed in human atria. Co-immunoprecipitation analysis demonstrated an interaction of TRPC1 with STIM1 and/or Orai1. Interestingly, protein expression of TRPC1 and STIM1, but not Orai1, was upregulated in human atria with atrial fibrillation. Our results indicate that the novel information that TRPC1 channels not only mediate the nonselective cation current, but also is a component of SOCs in human atria. The upregulation of TRPC1 and STIM1 in human atria with atrial fibrillation may suggest that TRPC1 channels and SOCs are likely involved in the atrial electrical and/or structure remodeling in patients with atrial fibrillation. Copyright © 2011 Biophysical Society. Published by Elsevier Inc. All rights reserved.-
dc.languageengen_US
dc.publisherCell Press. The Journal's web site is located at http://www.cell.com/biophysj/-
dc.relation.ispartofBiophysical Journalen_US
dc.titleTRPC1 channels mediate the nonselective cation current and store-operated calcium channels in human atrial myocytesen_US
dc.typeConference_Paperen_US
dc.identifier.emailSun, H: hysun@hkucc.hku.hken_US
dc.identifier.emailLi, GR: grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.bpj.2011.11.2917-
dc.identifier.hkuros199012en_US
dc.identifier.volume102en_US
dc.identifier.issue3, S1-
dc.identifier.spage534aen_US
dc.identifier.epage534aen_US
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats