中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Modulation of Ca2+ release through ryanodine receptors in vascular smooth muscle by protein kinase C alpha

文献类型:期刊论文

作者Peng, HongLi1; Yaney, Gordon C.3,4; Kirber, Michael T.2,4
刊名PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
出版日期2010-09
卷号460期号:4页码:791-802
关键词Protein kinase C Ryanodine receptor Calcium Caffeine
ISSN号0031-6768
DOI10.1007/s00424-010-0850-0
文献子类Article
英文摘要The role of protein kinase C (PKC) in Ca2+ release through ryanodine receptors (RyRs) in the sarcoplasmic reticulum (SR) of vascular smooth muscle cells (SMCs) is not well understood. Caffeine was used to activate RyRs and the intracellular Ca2+ concentration ([Ca2+](i)) was measured in both freshly isolated and cultured mouse aortic SMCs (ASMCs). Pre-activation of PKC with 1,2-dioctanoyl-sn-glycerol (DOG) prevented caffeine-induced [Ca2+](i) transients. Application of the PKC inhibitor calphostin C caused [Ca2+](i) transients which were not blocked by nifedipine or by removing extracellular Ca2+ but were abolished after inhibition of the SR Ca2+-ATPase with thapsigargin or after inhibition of RyRs with ryanodine. In addition, chelerythrine and GF109203X also elevated resting [Ca2+](i) but no further [Ca2+](i) increase was seen with subsequent application of caffeine. Selective inhibition of PKC alpha with safingol blocked caffeine-induced [Ca2+](i) transients, but the PKC epsilon inhibitory peptide V1-2 did not. In cells expressing a EGFP-tagged PKC alpha, caffeine-induced [Ca2+](i) transients were associated with a rapid focal translocation near the cell periphery, while application of ionomycin and DOG caused translocation to the plasma membrane. Western blot showed that caffeine increased the relative amount of PKC alpha in the particulate fraction in a time-dependent manner. Co-immunoprecipitation of RyRs and PKC alpha indicated that they interact. In conclusion, our studies suggest that PKC activation can inhibit the gating activity of RyRs in the SR of ASMCs, and this regulation is most likely mediated by the Ca2+-dependent PKC alpha isoform.
WOS关键词SKELETAL-MUSCLE ; INTRACELLULAR CALCIUM ; SARCOPLASMIC-RETICULUM ; SIGNAL-TRANSDUCTION ; INDUCED CONTRACTION ; HUMAN-NEUTROPHILS ; IN-SITU ; CELLS ; PHOSPHORYLATION ; ACTIVATION
资助项目National Natural Science Foundation of China[30672467] ; Ministry of Science and Technology[2007AA02Z308] ; American Diabetes Association[7-05-JF-53] ; NIH[DK35914] ; NIH[DK47223] ; Evans Department of Medicine, Boston University School of Medicine[00000000]
WOS研究方向Physiology
语种英语
WOS记录号WOS:000280920900010
出版者SPRINGER
源URL[http://119.78.100.183/handle/2S10ELR8/278792]  
专题药物化学研究室
中科院受体结构与功能重点实验室
新药研究国家重点实验室
通讯作者Kirber, Michael T.
作者单位1.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China;
2.Boston Univ, Med Ctr, Whitaker Cardiovasc Inst, Boston, MA 02118 USA;
3.Boston Univ, Med Ctr, Obes Res Ctr, Boston, MA 02118 USA;
4.Boston Univ, Med Ctr, Dept Med, Sect Mol Med, Boston, MA 02118 USA
推荐引用方式
GB/T 7714
Peng, HongLi,Yaney, Gordon C.,Kirber, Michael T.. Modulation of Ca2+ release through ryanodine receptors in vascular smooth muscle by protein kinase C alpha[J]. PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY,2010,460(4):791-802.
APA Peng, HongLi,Yaney, Gordon C.,&Kirber, Michael T..(2010).Modulation of Ca2+ release through ryanodine receptors in vascular smooth muscle by protein kinase C alpha.PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY,460(4),791-802.
MLA Peng, HongLi,et al."Modulation of Ca2+ release through ryanodine receptors in vascular smooth muscle by protein kinase C alpha".PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY 460.4(2010):791-802.

入库方式: OAI收割

来源:上海药物研究所

浏览0
下载0
收藏0
其他版本

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。