miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway
Autor: | Quan He, Jin-Juan Zhang, Xin-Hua Tang, Wen Zhang |
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Rok vydání: | 2020 |
Předmět: |
Pharmacology
education.field_of_study Messenger RNA medicine.diagnostic_test business.industry Population CD34 030209 endocrinology & metabolism Transfection 030204 cardiovascular system & hematology Flow cytometry 03 medical and health sciences 0302 clinical medicine Western blot Apoptosis Internal Medicine Cancer research Medicine Signal transduction business education |
Zdroj: | Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 13:4435-4446 |
ISSN: | 1178-7007 |
Popis: | Purpose A majority of diabetes mellitus patients with disturbances of glucose metabolism present with vascular complications. This study aimed to explore regulatory mechanisms of miR145 and its potential target gene ANGPT2 on diabetic vasculopathy under hyperglycemia. Methods Based on the fact that miR145 is detected in rat aortic endothelial cells (RAECs) under hyperglycemia, RAECs were transfected with miR145 mimics/inhibitor for further confirmation. RAEC proliferation was detected with CCK8 assays, and cell apoptosis and CD34+-cell population with annexinV-PI staining and anti-CD34FITC on flow cytometry, respectively. Then, qPCR and Western blot were applied to detect mRNA and protein expression of ANGPT2 and involved pathway factor NFκB p65. Subsequently, dual luciferase-reporter gene analysis was utilized to verify whether miR145 acted directly upon the 3'UTR of ANGPT2 mRNA. Results The ANGPT2 gene was confirmed to be a direct target of miR145. miR145 mimics markedly downregulated the expression of ANGPT2 and NFκB p65, boosted the percentage of the CD34+ phenotype, and promoted proliferation and suppressed apoptosis of RAECs under hyperglycemia. Conclusion miR145 might regulate the viability of RAECs via targeting ANGPT2 and involving NFκB signaling to exert a protective effect on diabetic vasculature. |
Databáze: | OpenAIRE |
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