| Ca2+/CaM-CaN 途径参与神经肽Y 诱导的大鼠心肌细胞肥大 |
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| 引用本文： | 董颀,陈敏生,李晓云,黄少华,李荧辉,张舒,刘振秀.Ca2+/CaM-CaN 途径参与神经肽Y 诱导的大鼠心肌细胞肥大[J].金属学报,2005,10(1):65-68. |
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| 作者姓名： | 董颀 陈敏生 李晓云 黄少华 李荧辉 张舒 刘振秀 |
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| 作者单位： | 广州医学院生理教研室, ;1.第二附属医院心血管内科, ;2.学报编辑部, 广州 510182, 广东;3.航天医学工程研究所, 北京 100094;4.第四军医大学航空生理系, 西安 710054, 陕西 |
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| 基金项目： | 广东省自然科学基金资助项目(No980466) |
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| 摘 要： | 目的: 探讨Ca2+ CaM 依赖的钙调神经磷酸酶(CaN) 途径在神经肽Y(NPY) 诱导心肌细胞肥大中的作用。方法: 用NPY (10、100 nmol·L-1) 刺激WISTAR 乳鼠心肌细胞, 并用CaN 特异性抑制剂环胞霉素A 加以干预。应用3H-Leu 掺入法测定心肌细胞蛋白质合成速率, 用免疫印迹(Western-blot) 和组织化学法分别测定心肌细胞内CaN-α蛋白表达和CaN 酶的活性。结果: 较高浓度NPY(100 nmol·L-1) 可明显增加心肌细胞3H-Leu 掺入量(P < 0.05), 加入CsA 可阻断上述效应;NPY(100 nmol·L-1) 还可明显增加心肌细胞内CaN 酶比活性(P <0.05), 并刺激心肌细胞CaN-α蛋白表达(P <0.05) 。结论: NPY 可活化大鼠心肌细胞Ca2+CaM-CaN 途径, 而CaN 特异性抑制剂环胞霉素A 可抑制NPY 诱导的心肌肥大, 说明Ca2+ CaM 依赖的钙调神经磷酸酶(CaN) 途径参与神经肽Y 诱导的心肌细胞肥大效应。
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| 关 键 词： | 神经肽Y 钙调神经磷酸酶 胞霉素A 心肌细胞肥大 |
| 收稿时间： | 2004-11-09 |
| 修稿时间： | 2004-12-24 |
Effects of Ca2+ CaM-dependent calcineurin signaling pathway on cardiomyocytes hypertrophy of rats induced by neuropeptide Y |
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| DONG Qi,CHEN Min-sheng,HUANG Shao-hua,LI Xiao-yun,LI Ying-hui,ZHANG Shu,LIU Zhen-xiu.Effects of Ca2+ CaM-dependent calcineurin signaling pathway on cardiomyocytes hypertrophy of rats induced by neuropeptide Y[J].Acta Metallurgica Sinica,2005,10(1):65-68. |
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| Authors: | DONG Qi CHEN Min-sheng HUANG Shao-hua LI Xiao-yun LI Ying-hui ZHANG Shu LIU Zhen-xiu |
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| Affiliation: | Department of Physiology, ;1.Department of Cardiology, the Second Affiliated Hospital, ;2.Editory of Academic Journal, Guangzhou Medical College, Guangzhou 510260, Guangdong, China;3.Institute of Spaceflight Medical engine, Beijng 100094;4.Department of Spaceflight Physiology, the Forth Military Medical University, Xi'an 710054, Shannxi |
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| Abstract: | AIM: To investigate the effects of Ca2+ CaM-dependent calcineurin (CaN) signaling pathway on cardiomyocytes hypertrophy of rat induced by neuropeptide Y (NPY).METHODS: Cardiomyocytes of neonatal Wistar rats were cultured with NPY of various concentrations (10, 100 nmol·L-1).Cyclosporine A (CsA) was used to inhibit the activity of CaN.The methods of 3H-Leu incorporation was used to assess protein synthesis rate in cardiomyocytes.Western-blot and histochemistry were used to measure CaN protein expression and CaN activity in cardiomyocytes.RESULTS: 3H-Leu incorporation of cardiomyocytes were increased significantly by 100 nmol·L-1NPY (P <0.05) and decreased by CsA.CaN activity and CaN-αprotein expression was elevated markedly in cardiomyocytes by 100 nmol·L-1NPY (P < 0.05).CONCLUSION: Neuropeptide Y activates Ca2+ CaM-dependent calcineurin signal pathway, and CsA can inhibit cardiomyocytes hypertrophy induced by NPY. It indicates that Ca2+ CaM-dependent calcineurin (CaN) signaling pathway plays an important role in cardiomyocytes hypertrophy of rats induced by NPY. |
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| Keywords: | neuropeptide Y calcineurin cardiomyocytes hypertrophy |
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