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MHY1485通过激活mTOR-Nrf2信号通路改善紫外线诱导的皮肤细胞损伤。

MHY1485 ameliorates UV-induced skin cell damages via activating mTOR-Nrf2 signaling.

作者信息

Yang Bo, Xu Qiu-Yun, Guo Chun-Yan, Huang Jin-Wen, Wang Shu-Mei, Li Yong-Mei, Tu Ying, He Li, Bi Zhi-Gang, Ji Chao, Cheng Bo

机构信息

Department of Dermatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Department of Dermatology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.

出版信息

Oncotarget. 2017 Feb 21;8(8):12775-12783. doi: 10.18632/oncotarget.14299.

DOI:10.18632/oncotarget.14299
PMID:28061443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5355053/
Abstract

Ultra Violet (UV)-caused skin cell damage is a main cause of skin cancer. Here, we studied the activity of MHY1485, a mTOR activator, in UV-treated skin cells. In primary human skin keratinocytes, HaCaT keratinocytes and human skin fibroblasts, MHY1485 ameliorated UV-induced cell death and apoptosis. mTOR activation is required for MHY1485-induced above cytoprotective actions. mTOR kinase inhibitors (OSI-027, AZD-8055 and AZD-2014) or mTOR shRNA knockdown almost abolished MHY1485-induced cytoprotection. Further, MHY1485 treatment in skin cells activated mTOR downstream NF-E2-related factor 2 (Nrf2) signaling, causing Nrf2 Ser-40 phosphorylation, stabilization/upregulation and nuclear translocation, as well as mRNA expression of Nrf2-dictated genes. Contrarily, Nrf2 knockdown or S40T mutation almost nullified MHY1485-induced cytoprotection. MHY1485 suppressed UV-induced reactive oxygen species production and DNA single strand breaks in skin keratinocytes and fibroblasts. Together, we conclude that MHY1485 inhibits UV-induced skin cell damages via activating mTOR-Nrf2 signaling.

摘要

紫外线（UV）导致的皮肤细胞损伤是皮肤癌的主要原因。在此，我们研究了mTOR激活剂MHY1485在紫外线处理的皮肤细胞中的活性。在原代人皮肤角质形成细胞、HaCaT角质形成细胞和人皮肤成纤维细胞中，MHY1485减轻了紫外线诱导的细胞死亡和凋亡。MHY1485诱导的上述细胞保护作用需要mTOR激活。mTOR激酶抑制剂（OSI-027、AZD-8055和AZD-2014）或mTOR shRNA敲低几乎消除了MHY1485诱导的细胞保护作用。此外，在皮肤细胞中用MHY1485处理激活了mTOR下游的核因子E2相关因子2（Nrf2）信号通路，导致Nrf2丝氨酸40磷酸化、稳定/上调和核转位，以及Nrf2调控基因的mRNA表达。相反，Nrf2敲低或S40T突变几乎使MHY1485诱导的细胞保护作用无效。MHY1485抑制了紫外线诱导的皮肤角质形成细胞和成纤维细胞中的活性氧生成和DNA单链断裂。总之，我们得出结论，MHY1485通过激活mTOR-Nrf2信号通路抑制紫外线诱导的皮肤细胞损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/a61a043f4a26/oncotarget-08-12775-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/82dde99240e2/oncotarget-08-12775-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/20ef8d50aeba/oncotarget-08-12775-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/64880117c681/oncotarget-08-12775-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/46cb2e3269a9/oncotarget-08-12775-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/a61a043f4a26/oncotarget-08-12775-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/82dde99240e2/oncotarget-08-12775-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/20ef8d50aeba/oncotarget-08-12775-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/64880117c681/oncotarget-08-12775-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/46cb2e3269a9/oncotarget-08-12775-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b27/5355053/a61a043f4a26/oncotarget-08-12775-g005.jpg

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