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- Kim Mi Jeong
- Department of Physiology, School of Medicine, Ajou University
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- Moon Chang-Hyun
- Department of Physiology, School of Medicine, Ajou University
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- Kim Mi-Young
- Department of Physiology, School of Medicine, Ajou University
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- Kim Min Hwa
- Department of Physiology, School of Medicine, Ajou University
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- Lee Soo Hwan
- Department of Physiology, School of Medicine, Ajou University
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- Baik Eun Joo
- Department of Physiology, School of Medicine, Ajou University
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- Jung Yi-Sook
- Department of Physiology, School of Medicine, Ajou University
書誌事項
- タイトル別名
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- Role of PKC-.DELTA. during Hypoxia in Heart-Derived H9c2 Cells
- Role of PKC デルタ during Hypoxia in Heart Derived H9c2 Cells
この論文をさがす
説明
In the present study, we investigated the role of protein kinase C (PKC) isoforms during hypoxia in heart-derived H9c2 cells. Hypoxia caused a rapid translocation of PKC-δ from soluble to particulate fraction and a downregulation of PKC-ε and PKC-ζ, whereas PKC-α and PKC-βI remained unaltered. When H9c2 cells were pretreated with PKC-δ inhibitor rottlerin (3 μM), hypoxia-induced apoptotic and necrotic cell death were significantly increased. Hypoxic insult also caused an activation of extracellular signal-regulated protein kinase (ERK) and p38 MAPK with no change in c-Jun NH2-terminal protein kinase (JNK) phosphorylation. Hypoxia-induced cell death was increased by treatment with ERK1/2 inhibitor U0126 (10 μM), but attenuated by p38 MAPK inhibitor SB202190 (10 μM). Treatment with rottlerin completely blocked the hypoxia-induced ERK phosphorylation, whereas it significantly increased p38 MAPK phosphorylation. The hypoxia-induced translocation of PKC-δ was not altered by U0126 and/or SB202190. From these results, it is suggested that hypoxia causes a rapid translocation of PKC-δ and subsequently ERK activation and p38 inactivation, rendering H9c2 cells resistant to hypoxia-induced cell death.<br>
収録刊行物
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- The Japanese Journal of Physiology
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The Japanese Journal of Physiology 54 (4), 405-414, 2004
一般社団法人 日本生理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205043112960
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- NII論文ID
- 10014089807
- 30015530023
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- NII書誌ID
- AA00691224
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- ISSN
- 18811396
- 0021521X
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- NDL書誌ID
- 7197239
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- PubMed
- 15631696
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- 本文言語コード
- en
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- 資料種別
- journal article
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- データソース種別
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- JaLC
- NDLサーチ
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可