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Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes

  • Authors:
    • Wenzhong Zhou
    • Jian Yang
    • Di Zhang
    • Fengyin Li
    • Guo Li
    • Yanyun Gu
    • Min Luo
  • View Affiliations / Copyright

    Affiliations: Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Jiaotong University School of Medicine, Shanghai 200025, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 67-73
    |
    Published online on: April 22, 2015
       https://doi.org/10.3892/etm.2015.2439
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Abstract

Cardiovascular complications are the major causes of morbidity and mortality associated with Type 2 Diabetes. Among the macrovascular complications, diabetic cardiomyopathy (DCM) is generally considered to be inadequately recognized and managed. Bcl‑2/adenovirus E1B 19 kDa‑interacting protein 3 (BNIP3), is known to play a key role in the initiation of the mitochondrial pathway of apoptosis induced by hypoxia and acidosis in the heart. It is unknown whether BNIP3 is also important for cardiac cell survival or adaption in response to hyperglycemia. Based on the previous finding that BNIP3 was significantly induced in the diabetic rat heart, BNIP3 was transfected in primary rat cardiomyocytes and the H9c2 cell line in the present study. Overexpressed BNIP3 decreased the mitochondrial membrane potential and induced cell apoptosis. When BNIP3 was knocked down, the effect on cell apoptosis was reversed. Transcriptome analysis showed that the genes regulating mitochondrial metabolism, such as carnitine palmitoyltransferase 1b, cytochrome c oxidase subunit VIIIb and creatine kinase (brain), and those regulating cardiac fibrosis, such as matrix metallopeptidase 9, could be the targets of BNIP3 in rat cardiomyocytes. In conclusion, hyperglycemia‑induced BNIP3 expression may compromise cardiac cell survival and function. Under the diabetic condition, BNIP3 could be involved in the regulation of mitochondrial function, lipid metabolism and fibrosis. BNIP3 could therefore serve as a potential drug target against diabetic macrovascular complications and, in particular, DCM.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou W, Yang J, Zhang D, Li F, Li G, Gu Y and Luo M: Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes. Exp Ther Med 10: 67-73, 2015.
APA
Zhou, W., Yang, J., Zhang, D., Li, F., Li, G., Gu, Y., & Luo, M. (2015). Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes. Experimental and Therapeutic Medicine, 10, 67-73. https://doi.org/10.3892/etm.2015.2439
MLA
Zhou, W., Yang, J., Zhang, D., Li, F., Li, G., Gu, Y., Luo, M."Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes". Experimental and Therapeutic Medicine 10.1 (2015): 67-73.
Chicago
Zhou, W., Yang, J., Zhang, D., Li, F., Li, G., Gu, Y., Luo, M."Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes". Experimental and Therapeutic Medicine 10, no. 1 (2015): 67-73. https://doi.org/10.3892/etm.2015.2439
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou W, Yang J, Zhang D, Li F, Li G, Gu Y and Luo M: Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes. Exp Ther Med 10: 67-73, 2015.
APA
Zhou, W., Yang, J., Zhang, D., Li, F., Li, G., Gu, Y., & Luo, M. (2015). Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes. Experimental and Therapeutic Medicine, 10, 67-73. https://doi.org/10.3892/etm.2015.2439
MLA
Zhou, W., Yang, J., Zhang, D., Li, F., Li, G., Gu, Y., Luo, M."Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes". Experimental and Therapeutic Medicine 10.1 (2015): 67-73.
Chicago
Zhou, W., Yang, J., Zhang, D., Li, F., Li, G., Gu, Y., Luo, M."Role of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 in myocardial cells in diabetes". Experimental and Therapeutic Medicine 10, no. 1 (2015): 67-73. https://doi.org/10.3892/etm.2015.2439
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