Role of MiR-30a in cardiomyocyte autophagy induced by Angiotensin II
العنوان: | Role of MiR-30a in cardiomyocyte autophagy induced by Angiotensin II |
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المؤلفون: | Ximing Chen, Shiming Liu, Chunlin Huang, Jionghua Huang, Yishan Luo |
المصدر: | Journal of the Renin-Angiotensin-Aldosterone System, Vol 16 (2015) |
بيانات النشر: | Hindawi Limited, 2014. |
سنة النشر: | 2014 |
مصطلحات موضوعية: | Autophagosome, Medicine (General), medicine.medical_specialty, Heart Diseases, In Vitro Techniques, Biology, Protein expression, R5-920, Endocrinology, Downregulation and upregulation, Internal medicine, Autophagy, Internal Medicine, medicine, Animals, Myocytes, Cardiac, Animal study, L-Lactate Dehydrogenase, Angiotensin II, Molecular biology, Cell Hypoxia, Rats, Cell biology, Blot, MicroRNAs, Protein regulation, Beclin-1, Apoptosis Regulatory Proteins |
الوصف: | Objective: The aim of this study was to investigate whether MiR-30a regulates autophagy by regulating the Beclin-1 protein, which is the marker for autophagosomes during myocardial injury, when induced by angiotensin II (Ang II). Methods: We randomly assigned 20 rats into two equal groups: Control group and Ang II group. We detected the expression of MiR-30a by quantitative real-time polymerase chain reaction (RT-PCR), and we employed western blotting to detect the protein expression of Beclin-1. Results: In this study, we found that Ang II induced cardiomyocyte autophagy, together with down-regulation of MiR-30a and upregulation of the Beclin-1 protein. We also found that the Beclin-1 protein is regulated by MiR-30a, by transferring a MiR-30a mimic or AMO-204 into the cardiomyocytes. Conclusion: These studies provided evidence that MiR-30a plays an important role in regulating autophagy through the Beclin-1 protein, during myocardial injury induced by Ang II. |
تدمد: | 1752-8976 1470-3203 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::52a8ef71d8a472f6f1bd0549ac12be16Test https://doi.org/10.1177/1470320314562060Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....52a8ef71d8a472f6f1bd0549ac12be16 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 17528976 14703203 |
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