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Title: | miR-21-5p Under-Expression in Patients with Obstructive Sleep Apnea Modulates Intermittent Hypoxia with Re-Oxygenation-Induced-Cell Apoptosis and Cytotoxicity by Targeting Pro-Inflammatory TNF-alpha-TLR4 Signaling |
Authors: | Chen, YC;Hsu, PY;Su, MC;Chin, CH;Liou, CW;Wang, TY;Lin, YY;Lee, CP;Lin, MC;Hsiao, CC |
Keywords: | obstructive sleep apnea;miR-21-5p;miR-23a-3p;apoptosis;intermittent hypoxia with re-oxygenation |
Date: | 2020 |
Issue Date: | 2022-08-09T08:03:51Z (UTC)
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Publisher: | MDPI |
Abstract: | The purpose of this study is to explore the anti-inflammatory role of microRNAs (miR)-21 and miR-23 targeting the TLR/TNF-alpha pathway in response to chronic intermittent hypoxia with re-oxygenation (IHR) injury in patients with obstructive sleep apnea (OSA). Gene expression levels of the miR-21/23a, and their predicted target genes were assessed in peripheral blood mononuclear cells from 40 treatment-naive severe OSA patients, and 20 matched subjects with primary snoring (PS). Human monocytic THP-1 cell lines were induced to undergo apoptosis under IHR exposures, and transfected with miR-21-5p mimic. Both miR-21-5p and miR-23-3p gene expressions were decreased in OSA patients as compared with that in PS subjects, while TNF-alpha gene expression was increased. Both miR-21-5p and miR-23-3p gene expressions were negatively correlated with apnea hypopnea index and oxygen desaturation index, while TNF-alpha gene expression positively correlated with apnea hypopnea index. In vitro IHR treatment resulted in decreased miR-21-5p and miR-23-3p expressions. Apoptosis, cytotoxicity, and gene expressions of their predicted target genes-including TNF-alpha, ELF2, NFAT5, HIF-2 alpha, IL6, IL6R, EDNRB, and TLR4-were all increased in response to IHR, while all were reversed with miR-21-5p mimic transfection under IHR condition. The findings provide biological insight into mechanisms by which IHR-suppressed miRs protect cell apoptosis via inhibit inflammation, and indicate that over-expression of the miR-21-5p may be a new therapy for OSA. |
URI: | http://dx.doi.org/10.3390/ijms21030999 https://www.webofscience.com/wos/woscc/full-record/WOS:000522551605038 https://ir.csmu.edu.tw:8080/handle/310902500/24529 |
Relation: | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES ,2020 ,v21 ,issue 3 |
Appears in Collections: | [中山醫學大學研究成果] 期刊論文
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