Expression of T-type Ca〔2+〕 Channels in Fetal and Diseased Heart

• Yasui Kenji

  Department of Bioinformation Analysis, Research Institute of Environmental Medicine, Nagoya University

• Niwa Noriko

  Department of Circulation, Research Institute of Environmental Medicine, Nagoya University

• Takemura Haruki

  Department of Cardio-Thoracic Surgery, Nagoya University Graduate School of Medicine

• Opthof Tobias

  Experimental and Molecular Cardiology Groups, Academic Medical Center Department of Medical Physiology, University Medical Center Utrecht

• Muto Takao

  Department of Circulation, Research Institute of Environmental Medicine, Nagoya University

• Horiba Mitsuru

  Department of Circulation, Research Institute of Environmental Medicine, Nagoya University

• Shimizu Atsuya

  Department of Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University

• Lee Jong-Kook

  Department of Circulation, Research Institute of Environmental Medicine, Nagoya University

• Honjo Haruo

  Department of Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University

• Kamiya Kaichiro

  Department of Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University

• Kodama Itsuo

  Department of Circulation, Research Institute of Environmental Medicine, Nagoya University

書誌事項

タイトル別名

• Pathophysiological Significance of T-type Ca2+ Channels: Expression of T-type Ca2+ Channels in Fetal and Diseased Heart
• Expression of T type Ca 2 Channels in Fetal and Diseased Heart

抄録

Re-expression of fetal genes has been considered to underlie ionic remodeling in diseased heart. T-type Ca²⁺ channels have been reported to be functionally expressed in embryonic hearts. In this review, we summarize developmental changes of T-type Ca²⁺ channels in mouse ventricles from 9.5 days postcoitum (dpc) to adulthood, using patch clamp and quantitative PCR. In addition, we introduced T-type Ca²⁺ channel expression in hypertrophied ventricles caused by myocardial infarction (MI) and aortic banding (AOB). Substantial T-type Ca²⁺ channel current was recorded at both 9.5 and 18 dpc. The currents were inhibited by Ni²⁺ at low concentrations. The current was not detectable in the adult stage. Ca_v3.2 (α_1H) mRNA is expressed dominantly at both 9.5 and 18 dpc. Ca_v3.1 (α_1G) increases from 9.5 to 18 dpc, but remains at low level compared with Ca_v3.2. In contrast, Ca_v3.1 is greater than Ca_v3.2 at the adult stage. In MI, Ca_v3.1 mRNA correlates negatively with brain natriuretic peptide (BNP) mRNA, whereas Ca_v3.2 mRNA correlates positively with BNP mRNA. In AOB, these correlations are weak. We also analyzed the neuron-restrictive silencer factor (NRSF) in these hearts because it is the suppressor of transcription of the fetal cardiac gene program. The negative correlation between NRSF and BNP was stronger in MI than in AOB. Our findings show that Ca_v3.2 underlies the functional T-type Ca²⁺ channel in embryonic heart and suggest that NRSF may regulate Ca_v3.2 expression in diseased hearts.<br>

収録刊行物

• Journal of Pharmacological Sciences

  Journal of Pharmacological Sciences 99 (3), 205-210, 2005

  公益社団法人 日本薬理学会

キーワード

• T-type Ca²⁺ channel
• gene expression
• embryonic heart
• development
• myocardial infarction

詳細情報

• CRID: 1390001205175762560
• NII論文ID: 10025730990
• NII書誌ID: AA11806667
• DOI: 10.1254/jphs.fmj05002x3
• COI: 1:CAS:528:DC%2BD2MXht1yntrvK
• ISSN: 13478648
• ISSN: 13478613
• NDL書誌ID: 7709898
• PubMed: 16272790
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I7709898
• Web Site: https://search.jamas.or.jp/link/ui/2006294910
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
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