Inhibition of miR‑186‑5p contributes to high glucose‑induced injury in AC16 cardiomyocytes

Jiang,Jiamei; Mo,Hailiang; Liu,Chang; Wu,Bin; Wu,Zijun; Li,Xingyue; Li,Teng; He,Songjian; Li,Shanghai; You,Qiong; Wu,Keng; Guo,Runmin

doi:10.3892/etm.2017.5445

January-2018 Volume 15 Issue 1

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January-2018 Volume 15 Issue 1

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Article Open Access

Inhibition of miR‑186‑5p contributes to high glucose‑induced injury in AC16 cardiomyocytes

Authors:
- Jiamei Jiang
- Hailiang Mo
- Chang Liu
- Bin Wu
- Zijun Wu
- Xingyue Li
- Teng Li
- Songjian He
- Shanghai Li
- Qiong You
- Keng Wu
- Runmin Guo
View Affiliations / Copyright

Affiliations: Department of Cardiology, The Affiliated Hospital, Guangdong Medical University, Zhanjiang, Guangdong 524001, P.R. China

Copyright: © Jiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 627-632
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Published online on: November 6, 2017

https://doi.org/10.3892/etm.2017.5445
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Abstract

A growing body of evidence has demonstrated that microRNAs (miRs) have pivotal roles in the pathophysiological development mechanisms of diabetic cardiomyopathy (DCM). Previous studies have demonstrated that miR‑186‑5p was significantly decreased in DCM. In addition, it has recently been reported that an imbalance of miR‑186 is associated with a variety of physiological and pathological processes. Therefore, the present study was designed to investigate the role of miR‑186‑5p in high glucose (HG)‑induced cytotoxicity and apoptosis in AC16 cardiomyocytes. Reverse transcription‑polymerase chain reaction was used to demonstrate the significant decrease in the level of miR‑186‑5p in HG‑treated AC16 cells (P<0.05). Subsequently, it was clarified that pre‑transfection with miR‑186‑5p mimic significantly ameliorated the effects of high glucose, which induced a significant decrease in the viability of AC16 cells (P<0.05) and increases in apoptosis, as evidenced by the appearance of apoptotic nucleus and the significant upregulation of apoptosis rate in AC16 cells (P<0.05). In addition, the significantly increased expression of caspase‑3 induced by HG (P<0.01) was also reversed by miR‑186‑5p mimic (P<0.01). Conversely, transfection with miR‑186‑5p inhibitor significantly reduced the viability of AC16 cells (P<0.05) and promoted apoptosis (P<0.05) as well as the expression of caspase‑3 in AC16 cells (P<0.01), indicating the beneficial role of miR‑186‑5p in the physiological process of HG‑induced damage. In conclusion, these results suggest that the distribution of miR‑186‑5p contributes to HG‑induced cytotoxicity and apoptosis in AC16 cardiomyocytes.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Inhibition of miR‑186‑5p contributes to high glucose‑induced injury in AC16 cardiomyocytes

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