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褪黑素通过上调Sestrin2抑制血管平滑肌细胞增殖和凋亡。

Melatonin inhibits vascular smooth muscle cell proliferation and apoptosis through upregulation of Sestrin2.

作者信息

Lee Seunghyeong, Byun Jun-Kyu, Park Mihyang, Woo Kim Sung, Lee Sungwoo, Kim Jung-Guk, Lee In-Kyu, Choi Yeon-Kyung, Park Keun-Gyu

机构信息

Department of Biomedical Science, Graduate School, Kyungpook National University, Daegu 41566, Republic of Korea.

BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41566, Republic of Korea.

出版信息

Exp Ther Med. 2020 Jun;19(6):3454-3460. doi: 10.3892/etm.2020.8638. Epub 2020 Apr 2.

DOI:10.3892/etm.2020.8638
PMID:32373191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7197251/
Abstract

Excessive vascular smooth muscle cell (VSMC) proliferation contributes to the development of atherosclerosis and restenosis. Furthermore, apoptosis of VSMCs accelerates plaque rupture in the atherosclerotic vessels. Therefore, a strategy that regulates both VSMC proliferation and apoptosis is essential for the development of novel pharmacological tools for the treatment of atherosclerosis. Despite mounting evidence supporting the benefits of melatonin in diverse metabolic diseases, the role of melatonin in VSMC growth remains largely unknown. The present study revealed that melatonin inhibited both proliferation and apoptosis of primary cultured rat VSMCs. Melatonin induced mitochondrial energetic stress in VSMCs and subsequent induction of Sestrin2 via C/EBPβ. Melatonin-induced Sestrin2 suppressed mTORC1 activity in VSMCs, contributing to suppression of VSMC proliferation. Additionally, melatonin-induced upregulation of Sestrin2 blocked apoptosis by preventing excessive ROS generation. The results demonstrated that melatonin controlled VSMC proliferation and apoptosis via Sestrin2-mediated inhibition of mTORC1 and ROS scavenging. Therefore, melatonin should be considered as a lead compound for therapies aimed at preventing vessel lumen constriction during the course of atherosclerosis and restenosis.

摘要

血管平滑肌细胞（VSMC）过度增殖会导致动脉粥样硬化和再狭窄的发展。此外，VSMC的凋亡会加速动脉粥样硬化血管中的斑块破裂。因此，一种既能调节VSMC增殖又能调节其凋亡的策略对于开发治疗动脉粥样硬化的新型药理学工具至关重要。尽管越来越多的证据支持褪黑素在多种代谢性疾病中的益处，但褪黑素在VSMC生长中的作用仍 largely unknown。本研究表明，褪黑素抑制原代培养的大鼠VSMC的增殖和凋亡。褪黑素在VSMC中诱导线粒体能量应激，并随后通过C/EBPβ诱导Sestrin2。褪黑素诱导的Sestrin2抑制VSMC中的mTORC1活性，有助于抑制VSMC增殖。此外，褪黑素诱导的Sestrin2上调通过防止过量ROS生成来阻止凋亡。结果表明，褪黑素通过Sestrin2介导的mTORC1抑制和ROS清除来控制VSMC增殖和凋亡。因此，褪黑素应被视为旨在预防动脉粥样硬化和再狭窄过程中血管腔狭窄的治疗的先导化合物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/40705eacbeee/etm-19-06-3454-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/e8f1e2cb0593/etm-19-06-3454-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/b497267138b5/etm-19-06-3454-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/3f4ff4b89ba1/etm-19-06-3454-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/40705eacbeee/etm-19-06-3454-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/e8f1e2cb0593/etm-19-06-3454-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/b497267138b5/etm-19-06-3454-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/3f4ff4b89ba1/etm-19-06-3454-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f840/7197251/40705eacbeee/etm-19-06-3454-g03.jpg

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