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Calcineurin-NFAT signaling is involved in phenylephrine-induced vascular smooth muscle cell proliferation
Pang, Xiao1,2; Sun, Ning-ling1
关键词Phenylephrine Calcineurin Nuclear Factor Of Activated t Cells Proliferation Vascular Smooth Muscle Cells
刊名ACTA PHARMACOLOGICA SINICA
2009-05-01
DOI10.1038/aps.2009.28
30期:5页:537-544
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]ACTIVATED T-CELLS ; RECEPTOR TYROSINE KINASE ; NUCLEAR FACTOR ; NEOINTIMA FORMATION ; CYCLOSPORINE-A ; CAROTID-ARTERY ; DNA-SYNTHESIS ; GROWTH-FACTOR ; RAT ; TRANSCRIPTION
英文摘要

Aim: Catecholamine-induced vascular smooth muscle cell (VSMC) proliferation is one of the major events in the pathogenesis of atherosclerosis and vascular remodeling. The calcineurin-NFAT pathway plays a role in regulating growth and differentiation in various cell types. We investigated whether the calcineurin-NFAT pathway was involved in the regulation of phenylephrine-induced VSMC proliferation.

Methods: Proliferation of VSMC was measured using an MTT assay and cell counts. Localization of NFATc1 was detected by immunofluorescence staining. NFATc1-DNA binding was determined by EMSA and luciferase activity analyses. NFATc1 and calcineurin levels were assayed by immunoprecipitation.

Results: Phenylephrine (PE, an alpha(1)-adrenoceptor agonist) increased VSMC proliferation and cell number. Prazosin (an alpha(1)-adrenoceptor antagonist), cyclosporin A (CsA, an inhibitor of calcineurin) and chelerythrine (an inhibitor of PKC) decreased PE-induced proliferation and cell number. Additional treatment of VSMC with CsA or chelerythrine further inhibited proliferation and cell number in the chelerythrine-pretreatment group and the CsA-pretreatment group. CsA and chelerythrine alone had no effect on either absorbance or cell number. CsA decreased PE-induced calcineurin levels and activity. NFATc1 was translocated from the cytoplasm to the nucleus upon treatment with PE. This translocation was reversed by CsA. CsA decreased the PE-induced NFATc1 level in the nucleus. PE increased NFAT′s DNA binding activity and NFAT-dependent reporter gene expression. CsA blocked these effects.

Conclusion: CsA partially suppresses PE-induced VSMC proliferation by inhibiting calcineurin activity and NFATc1 nuclear translocation. The calcineurin-NFATc1 pathway is involved in the hyperplastic growth of VSMC induced by phenylephrine.

语种英语
WOS记录号WOS:000266015100005
引用统计
被引频次:14[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/400002259/56821
专题北京大学第二临床医学院_心血管内科
作者单位1.Peking Univ, Peoples Hosp, Dept Cardiol, Beijing 100044, Peoples R China
2.Xinjiang Shihezi Univ, Affiliated Hosp 1, Dept Geratol, Coll Med, Xinjiang 832008, Peoples R China
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GB/T 7714
Pang, Xiao,Sun, Ning-ling. Calcineurin-NFAT signaling is involved in phenylephrine-induced vascular smooth muscle cell proliferation[J]. ACTA PHARMACOLOGICA SINICA,2009,30(5):537-544.
APA Pang, Xiao,&Sun, Ning-ling.(2009).Calcineurin-NFAT signaling is involved in phenylephrine-induced vascular smooth muscle cell proliferation.ACTA PHARMACOLOGICA SINICA,30(5),537-544.
MLA Pang, Xiao,et al."Calcineurin-NFAT signaling is involved in phenylephrine-induced vascular smooth muscle cell proliferation".ACTA PHARMACOLOGICA SINICA 30.5(2009):537-544.
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