Differential Induction of Protein Kinase C Isoforms at the Cardiac Hypertrophy Stage and Congestive Heart Failure Stage in Dahl Salt-Sensitive Rats
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- KOIDE Yuichi
- Department of Medicine II, Yokohama City University School of Medicine Department of Molecular Biology, Yokohama City University School of Medicine
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- TAMURA Kouichi
- Department of Medicine II, Yokohama City University School of Medicine
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- SUZUKI Atsushi
- Department of Molecular Biology, Yokohama City University School of Medicine
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- KITAMURA Kouichi
- Department of Molecular Biology, Yokohama City University School of Medicine
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- YOKOYAMA Keiko
- Department of Medicine II, Yokohama City University School of Medicine
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- HASHIMOTO Tatsuo
- Department of Medicine II, Yokohama City University School of Medicine
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- HIRAWA Nobuhito
- Department of Medicine II, Yokohama City University School of Medicine
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- KIHARA Minoru
- Department of Medicine II, Yokohama City University School of Medicine
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- UMEMURA Satoshi
- Department of Medicine II, Yokohama City University School of Medicine
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Several protein kinase C (PKC) isoforms may play important roles in cellular signaling pathways. Recent reports have suggested that PKC plays critical isoform-specific roles in the development of cardiac hypertrophy and heart failure. The purpose of the present study was to examine the expression profiles of PKC isoforms in models of cardiac hypertrophy and heart failure. We examined the cardiac expression of individual PKC isoforms at the cardiac hypertrophy stage and the heart failure stage in Dahl salt-sensitive rats by Western blot analysis. The levels of all PKC isoforms increased at the cardiac hypertrophy stage and the heart failure stage, but the pattern of increase differed among PKC isoforms at the heart failure stage. The expressions of PKCα, β, and δ increased at the cardiac hypertrophy stage and remained elevated at the heart failure stage. On the other hand, the expression of PKCε and atypical PKCs (aPKCs) increased at the cardiac hypertrophy stage, but this increase tended to decline at the congestive heart failure stage. These results suggest that there are two groups of PKC isoforms. Several reports have shown that PKCα, β, and δ are involved in the development of cardiac hypertrophy and heart failure, and that PKCε plays a role in the physiological hypertrophic responses and cardioprotective actions. These facts suggest that all PKC isoforms (PKCα, β, δ, ε, and aPKCs) expressed in the heart may have similar functions at the cardiac hypertrophy stage, but that two groups of PKC isoforms (PKCα, β, δ, and PKCε, aPKCs) have different functions at the congestive heart failure stage. (Hypertens Res 2003; 26: 421-426)
収録刊行物
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- Hypertension Research
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Hypertension Research 26 (5), 421-426, 2003
日本高血圧学会
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詳細情報 詳細情報について
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- CRID
- 1390282679697441024
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- NII論文ID
- 130004437057
- 10011105910
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- NII書誌ID
- AA10847079
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- COI
- 1:CAS:528:DC%2BD3sXlvFCiu7o%3D
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- ISSN
- 13484214
- 09169636
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- PubMed
- 12887134
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 使用不可