miR-122 promotes diabetic retinopathy through targeting TIMP3
العنوان: | miR-122 promotes diabetic retinopathy through targeting TIMP3 |
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المؤلفون: | Jiwei Zhang, Guanghui Shao, Mingliang Wang, Xianbo Zhou, Huifen Zheng |
المصدر: | Animal Cells and Systems, Vol 24, Iss 5, Pp 275-281 (2020) Animal Cells and Systems article-version (VoR) Version of Record |
بيانات النشر: | Taylor & Francis Group, 2020. |
سنة النشر: | 2020 |
مصطلحات موضوعية: | 0301 basic medicine, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Diabetes mellitus, medicine, MiR-122, Viability assay, lcsh:QH301-705.5, cell viability, Gene knockdown, lcsh:R5-920, cell apoptosis, business.industry, Retinal, Diabetic retinopathy, medicine.disease, mir-122, timp3, diabetic retinopathy, 030104 developmental biology, chemistry, lcsh:Biology (General), Apoptosis, 030220 oncology & carcinogenesis, High glucose, Cancer research, Animal Science and Zoology, Molecular & Cellular Biology, business, lcsh:Medicine (General), Research Article |
الوصف: | Diabetic retinopathy (DR) is a primary complication of diabetes mellitus. DR can cause severe vision loss for patients. miR-122 is elevated in DR patients, while its role in DR is unclear. Hence, the purpose of this study was to analyze the effect of miR-122 on the function of high glucose-induced REC cells and the underlying molecular mechanisms. In this study, our results revealed that miR-122 was up-regulated in high glucose-induced human retinal pigment epithelial cells (ARPE-19). High glucose decreased the cell viability of ARPE-19 cells, which was then restored by miR-122 knockdown. In addition, miR-122 knockdown suppressed apoptosis of high glucose-induced ARPE-19 cells. High glucose also inhibited B-cell lymphoma-2 (Bcl-2) level and increased cleaved caspase-3 level in ARPE-19 cells, which were reversed by miR-122 knockdown. Tissue inhibitor of metalloproteinases-3 (TIMP3) was a direct target of miR-122. TIMP3 was decreased in high glucose-induced ARPE-19 cells, and the decrease was abrogated by miR-122 knockdown. In addition, the effects of miR-122 overexpression in cell viability and apoptosis of high glucose-induced ARPE-19 were abolished by overexpression of TIMP3. In conclusion, the effect and mechanism of miR-122 on high glucose-induced ARPE-19 cells were demonstrated for the first time. miR-122 promoted diabetic retinopathy through targeting TIMP3, making miR-122 a promising target for diabetic retinopathy therapy. |
اللغة: | English |
تدمد: | 2151-2485 1976-8354 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0e671958fcf4fb09965a90416022412bTest https://doaj.org/article/c98446dd69c84d789436aeb1b6781730Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....0e671958fcf4fb09965a90416022412b |
قاعدة البيانات: | OpenAIRE |
تدمد: | 21512485 19768354 |
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