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学科主题临床医学
Regulation of intracellular Ca2(+) and calcineurin by NO/PKG in proliferation of vascular smooth muscle cells
Li, SJ; Sun, NL
关键词cacium calcineurin nitric oxide cGMP-dependent protein kinase vascular smooth muscle
刊名ACTA PHARMACOLOGICA SINICA
2005-03-01
DOI10.1111/j.1745-7245.2005.00049.x
26期:3页:323-328
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Chemistry, Multidisciplinary ; Pharmacology & Pharmacy
研究领域[WOS]Chemistry ; Pharmacology & Pharmacy
关键词[WOS]DEPENDENT PROTEIN-KINASE ; CA2+ SENSITIZATION ; CARDIAC MYOCYTES ; NITRIC-OXIDE ; TRANSCRIPTION ; INHIBITION ; ACTIVATION ; MECHANISMS
英文摘要

Aim: To determine whether Ca2+/calcineurin mediated the inhibitory effects of nitric oxide /cGMP-dependent protein kinase (NO/PKG) on the proliferation of vascular smooth muscle cells (VSMC). Methods: Proliferation and viability of primary VSMC from rat aorta were measured using [3-(4,5-dimethyl thiazol-2-yl)-2, 5-diphenyl tetrazolium bromide] (MTT) assay and acridine orange and ethidium bromide staining, respectively. Cytosolic Ca2+ was determined by Fluo-3/AM. Calcineurin protein and its activity were assayed using immunoblotting and free inorganic phosphate analysis, respectively. Results: (+/-)-S-nitroso-N-acetylpenicillamine (SNAP) and Sp-8-(4-chlorophenylthio)-guanosine-3′,5′-cyclic monophosphorothioate (Sp-8-pCPT-cGMPS) decreased phenylephrine (PE)-induced proliferation of VSMC by 27.3% and 36.6%, respectively, but Rp-8-[4-chlorophenyl)thio]-guanosine-3′,5′-cyclic monophosphorothioate (Rp-8-pCPT-cGMPS) increased PE-induced proliferation of VSMC. SNAP, Sp-8-pCPT-cGMPS, and Rp-8-pCPT-cGMPS did not affect the viability of VSMC. Calcineurin protein was decreased by 63.1% and its activity was decreased by 59.7% in smooth muscle cells (SMC) pretreated with verapamil (Ver) and then stimulated by PE. In SMC pretreated with Ver, the absorbance of cells stimulated by PE decreased by 22.0% and was further inhibited by the additional treatment of SNAP and Sp-8-pCPT-cGMPS. In SMC pretreated with cyclosporin A (CsA), the absorbance of cells stimulated by PE decreased by 36.7%, but could not be further altered by the additional treatment of SNAP, Sp-8-pCPT-cGMPS, and Rp-8-pCPT-cGMPS. In addition, Ver inhibited PE-induced intracellular Ca 2, variations, which could be further inhibited by SNAP and Sp-8-pCPT-cGMPS, but not by Rp-8-pCPT-cGMPS. Moreover, the increase in calcineurin activity induced by PE was inhibited by SNAP and Sp-8-pCPT-cGMPS, but was promoted by Rp-8-pCPT-cGMPS. Conclusion: NO/PKG regulates calcineurin activity via the modulation of intracellular Ca 2, concentration, and thus partially inhibits the proliferation of VSMC without affecting their viability.

语种英语
WOS记录号WOS:000227647800010
引用统计
被引频次:13[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62907
专题北京大学第二临床医学院_心血管内科
作者单位Peking Univ, Dept Cardiol, Peoples Hosp, Beijing 100044, Peoples R China
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GB/T 7714
Li, SJ,Sun, NL. Regulation of intracellular Ca2(+) and calcineurin by NO/PKG in proliferation of vascular smooth muscle cells[J]. ACTA PHARMACOLOGICA SINICA,2005,26(3):323-328.
APA Li, SJ,&Sun, NL.(2005).Regulation of intracellular Ca2(+) and calcineurin by NO/PKG in proliferation of vascular smooth muscle cells.ACTA PHARMACOLOGICA SINICA,26(3),323-328.
MLA Li, SJ,et al."Regulation of intracellular Ca2(+) and calcineurin by NO/PKG in proliferation of vascular smooth muscle cells".ACTA PHARMACOLOGICA SINICA 26.3(2005):323-328.
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