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微小RNA-21抑制瘢痕疙瘩中线粒体介导的细胞凋亡。

MicroRNA-21 inhibits mitochondria-mediated apoptosis in keloid.

作者信息

Wu Hao, Wang Jie, Ma Hui, Xiao Zhibo, Dong Xiaoqun

机构信息

Department of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Department of Orthopaedics, The First Affiliated Hospital of General Hospital of The People's Liberation Army, Beijing, China.

出版信息

Oncotarget. 2017 Oct 6;8(54):92914-92925. doi: 10.18632/oncotarget.21656. eCollection 2017 Nov 3.

DOI:10.18632/oncotarget.21656
PMID:29190966
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5696232/
Abstract

MicroRNA-21 acts as an oncogene by promoting cell proliferation and migration, whereas inhibiting apoptosis in majority of cancers. MicroRNA-21 is upregulated in human keloid fibroblasts. We hypothesized that microRNA-21 may contribute to pathogenesis of keloid fibroblasts. First, enhanced miR-21 but reduced mitochondrial-mediated apoptosis observed in keloid tissues indicated its importance in keloids development. Second, upregulation of microRNA-21 induced a decrease in the ratio of BAX to BCL-2 and suppressed mitochondrial fission in keloid fibroblasts. Third, by attenuating the decline in cellular mitochondrial membrane potential, overexpression of miR-21 suppressed cytochrome c release to the cytoplasm, followed by a decrease in the activity of intracellular caspase-9 and caspase-3, suggesting that mitochondrial-mediated proapoptotic pathway was impaired. Simultaneously, intracellular reactive oxygen species were decreased, indicating microRNA-21 undermined oxidative stress. This phenotype was reversed by miR-21 inhibition. Therefore, our study demonstrates that inhibition of microRNA-21 induces mitochondrial-mediated apoptosis in keloid fibroblasts, proposing microRNA-21 as a potential therapeutic target in keloid fibroblasts.

摘要

微小RNA-21通过促进细胞增殖和迁移发挥癌基因作用，在大多数癌症中抑制细胞凋亡。微小RNA-21在人瘢痕疙瘩成纤维细胞中上调。我们推测微小RNA-21可能参与瘢痕疙瘩成纤维细胞的发病机制。首先，瘢痕疙瘩组织中观察到微小RNA-21增强但线粒体介导的细胞凋亡减少，表明其在瘢痕疙瘩形成中的重要性。其次，微小RNA-21的上调导致瘢痕疙瘩成纤维细胞中BAX与BCL-2的比例降低，并抑制线粒体分裂。第三，通过减弱细胞线粒体膜电位的下降，微小RNA-21的过表达抑制了细胞色素c释放到细胞质中，随后细胞内caspase-9和caspase-3的活性降低，表明线粒体介导的促凋亡途径受损。同时，细胞内活性氧减少，表明微小RNA-21削弱了氧化应激。这种表型通过抑制微小RNA-21得以逆转。因此，我们的研究表明，抑制微小RNA-21可诱导瘢痕疙瘩成纤维细胞中线粒体介导的细胞凋亡，提示微小RNA-21作为瘢痕疙瘩成纤维细胞潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/0590adf41aab/oncotarget-08-92914-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/6b637d7c812f/oncotarget-08-92914-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/a412ab084180/oncotarget-08-92914-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/7ddc4fa670d2/oncotarget-08-92914-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/e2879b1a21ed/oncotarget-08-92914-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/0590adf41aab/oncotarget-08-92914-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/6b637d7c812f/oncotarget-08-92914-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/a412ab084180/oncotarget-08-92914-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/7ddc4fa670d2/oncotarget-08-92914-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/e2879b1a21ed/oncotarget-08-92914-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/5696232/0590adf41aab/oncotarget-08-92914-g005.jpg

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