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瞬时受体电位通道蛋白1/瞬时受体电位通道蛋白3通道介导溶血磷脂酰胆碱诱导的人冠状动脉平滑肌细胞凋亡。

TRPC1/TRPC3 channels mediate lysophosphatidylcholine-induced apoptosis in cultured human coronary artery smooth muscles cells.

作者信息

Wang Yuan, Wang Yan, Li Gui-Rong

机构信息

Xiamen Cardiovascular Hospital, Medical School of Xiamen University, Xiamen, Fujian, China.

Department of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong, China.

出版信息

Oncotarget. 2016 Aug 9;7(32):50937-50951. doi: 10.18632/oncotarget.10853.

DOI:10.18632/oncotarget.10853
PMID:27472391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5239449/
Abstract

The earlier study showed that lysophosphatidylcholine (lysoPC) induced apoptosis in human coronary artery smooth muscle cells (SMCs); however, the related molecular mechanisms are not fully understood. The present study investigated how lysoPC induces apoptosis in cultured human coronary artery SMCs using cell viability assay, flow cytometry, confocal microscopy, and molecular biological approaches. We found that lysoPC reduced cell viability in human coronary artery SMCs by eliciting a remarkable Ca2+ influx. The effect was antagonized by La3+, SKF-96365, or Pyr3 as well as by silencing TRPC1 or TRPC3. Co-immunoprecipitation revealed that TRPC1 and TRPC3 had protein-protein interaction. Silencing TRPC1 or TRPC3 countered the lysoPC-induced increase of Ca2+ influx and apoptosis, and the pro-apoptotic proteins Bax and cleaved caspase-3 and decrease of the anti-apoptotic protein Bcl-2 and the survival kinase pAkt. These results demonstrate the novel information that TRPC1/TRPC3 channels mediate lysoPC-induced Ca2+ influx and apoptosis via activating the pro-apoptotic proteins Bax and cleaved caspase-3 and inhibiting the anti-apoptotic protein Bcl-2 and the survival kinase pAkt in human coronary artery SMCs, which implies that TRPC1/TRC3 channels may be the therapeutic target of lysoPC-induced disorders such as atherosclerosis.

摘要

早期研究表明，溶血磷脂酰胆碱（lysoPC）可诱导人冠状动脉平滑肌细胞（SMCs）凋亡；然而，相关分子机制尚未完全明确。本研究采用细胞活力测定、流式细胞术、共聚焦显微镜和分子生物学方法，研究lysoPC如何诱导培养的人冠状动脉SMCs凋亡。我们发现，lysoPC通过引发显著的Ca2+内流降低人冠状动脉SMCs的细胞活力。La3+、SKF-96365或Pyr3以及沉默TRPC1或TRPC3可拮抗该效应。免疫共沉淀显示TRPC1和TRPC3存在蛋白质-蛋白质相互作用。沉默TRPC1或TRPC3可对抗lysoPC诱导的Ca2+内流增加和凋亡，以及促凋亡蛋白Bax和裂解的caspase-3的增加，抗凋亡蛋白Bcl-2和存活激酶pAkt的减少。这些结果证明了新的信息，即TRPC1/TRPC3通道通过激活促凋亡蛋白Bax和裂解的caspase-3以及抑制抗凋亡蛋白Bcl-2和存活激酶pAkt介导lysoPC诱导的Ca2+内流和凋亡，这意味着TRPC1/TRC3通道可能是lysoPC诱导的疾病如动脉粥样硬化的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/d92e9cb55e1f/oncotarget-07-50937-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/7f40da39a9bf/oncotarget-07-50937-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/102af54d20f1/oncotarget-07-50937-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/537ad39cf450/oncotarget-07-50937-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/84f34dfa1fd3/oncotarget-07-50937-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/11166645ca05/oncotarget-07-50937-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/071e11c86098/oncotarget-07-50937-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/04681c7e920e/oncotarget-07-50937-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/d92e9cb55e1f/oncotarget-07-50937-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/7f40da39a9bf/oncotarget-07-50937-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/102af54d20f1/oncotarget-07-50937-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/537ad39cf450/oncotarget-07-50937-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/84f34dfa1fd3/oncotarget-07-50937-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/11166645ca05/oncotarget-07-50937-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/071e11c86098/oncotarget-07-50937-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/04681c7e920e/oncotarget-07-50937-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32b3/5239449/d92e9cb55e1f/oncotarget-07-50937-g008.jpg

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