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|本期目录/Table of Contents|

醛固酮诱导心肌成纤维细胞增殖的信号转导(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第3期
页码:
269-271/276
栏目:
基础研究
出版日期:
2007-06-01

文章信息/Info

Title:
Aldosterone induceds proliferation of rat cardiac fibroblasts: the role of CaN, MAPK and PKC
作者:
杨大春1; 张鑫2; 杨永健2; 肖贞良1
成都军区总医院:1.ICU，2.心血管内科，四川 成都 610083
Author(s):
YANG Dachun1;  ZHANG Xin2; YANG Yongjian2;  XIAO Zhenliang1
1.Department of ICU, 2.Department of Cardiology, General Hospital of Chengdu Military Area Command, Chengdu 610083, Sichuan, China
关键词:
醛固酮; 心肌成纤维细胞; 钙调神经磷酸酶; 丝裂素活化蛋白激酶; 蛋白激酶C
Keywords:
aldosterone;  Fibroblasts;  Calcineurin;  Mitogen activated protein kinase;  Protein kinase C
分类号:
Q813.1
DOI:
-
文献标识码:
A
摘要:
目的 探讨钙调神经磷酸酶（CaN）、丝裂素活化蛋白激酶（MAPK）、蛋白激酶C（PKC）信号通路在醛固酮（aldosterone ，ALD）诱导的乳鼠心肌成纤维细胞（fibroblasts， FBs）增殖中的作用。方法 以培养的FBs为模型，以3H亮氨酸及3H胸腺嘧啶掺入量作为反映FBs增殖的指标，用ALD诱导FBs增殖，并检测FBs CaN、MAPK、PKC活性。结果 ALD呈浓度依赖性增高FBs蛋白及核酸合成速率；螺旋内酯（spironolactone，SPI）能明显阻断ALD诱导的FBs蛋白及核酸合成。ALD诱导组FBs CaN、MAPK、PKC活性明显升高，与对照组相比差异显著（P<0.05或P<0.01）。SPI能阻断ALD诱导的FBs CaN、MAPK、FBs PKC活性增高。结论 CaN、MAPK、PKC信号通路均参与了ALD诱导的FBs增殖。
Abstract:
AIM To study the role of calcineurin (CaN), mitogen activated protein kinase (MAPK) and protein kinase C dependent signaling pathway in aldosteroneinduced proliferation of rat cardiac fibroblasts (FBs). METHODS Cardiac fibroblasts (FBs) from neonatal rats were treated with aldosterone and the FBs proliferation and the activities of CaN, MAPK and PKC were examined. RESULTS Aldosterone significantly increased FBs proliferation in a dose dependent manner as evidenced by the increased synthesis rates of protein and nucleic acid. Such proliferation in FBs was accompanied with the increases in activities of CaN, MAPK and PKC. More importantly, spironolactone markedly attenuated aldosteroneinduced proliferation and inhibited the activities of CaN, MAPK and PKC in FBs. CONCLUSION aldosterone induces the proliferation in FBs via the signaling pathway of CaN, MAPK and PKC.

参考文献/References

［1］Gallagher AM,Bahnson TD,Yu H, et al.Species variability in angiotensin receptor expression by cultured cardiac fibroblasts and the fracted heart［J］. Am J Physiol, 1998, 274(3 pt 2): H801-H809.

［2］Wilkins BJ, Dai YS, Bueno OF, et al. Calcineruin/NFAT coupling participates in pathological， but not physiological, cardiac hypertrophy［J］. Circ Res, 2004,94(1): 110-118.

［3］Yatani A, Honda R, Tymitz KM, et al. Enhanced Ca2+ channel currents in cardiac hypertrophy induced by activation of calcineurindependent pathway［J］. J Mol Cell Cardiol， 2001, 33（2）: 249-259.

［4］Molkentin JD . Calcineurin and beyond: Cardiac hypertrophic signaling［J］. Circ Res, 2000, 87（9）: 731-738.

［5］陈东海，季乃军，童丽军，等.慢性心力衰竭患者血清醛固酮水平的变化及临床意义［J］.心脏杂志，2005，17（3）：256-257.

［6］周兴文，杨永健，张鑫，等.钙调神经磷酸酶参与心肌成纤维细胞的增殖［J］.心脏杂志，2002，14（3）：181-183.

［7］Meszaros JG, Raphael R, Lio FM, et al. Protein kinase C contributes to desensitization of ANGⅡ signaling in adult rat cardiac fibroblasts［J］. Am J Physiol Cell Physiol, 2000, 279(6): 1978-1985.

［8］Stockand JD, Meszaros JG. Aldstone stimulates proliferation of cardiac fibroblasts by activating Ki Ras A and MAPK1/2 signaling［J］. Am J Physiol Heart Circ Physiol, 2003, 284(1): H176-H184.

备注/Memo

备注/Memo:
收稿日期：2006-04-24.作者简介：杨大春，主治医师，硕士Email:yangdc71@126.com
更新日期/Last Update: