miR-483-3p regulates hyperglycaemia-induced cardiomyocyte apoptosis in transgenic mice

Biochemical and Biophysical Research Communications

Volumn 477, Issue 4, 2016, Pages 541-547

  Qiao, Yu ^a,e   Zhao, Yanli ^b   Liu, Yan ^a   Ma, Ning ^a,c   Wang, Chuxuan ^a   Zou, Jiaqi ^a,d   Liu, Zhiyan ^a,d   Zhou, Zhongqiu ^a,d   Han, Dong ^a   He, Jun ^a   Sun, Qian ^a   Liu, Yicong ^a   Xu, Changqing ^a   Du, Zhimin ^a,d   Huang, Hui ^a,e  

^a HARBIN MEDICAL UNIVERSITY   (China)

^b QINGHAI UNIVERSITY   (China)

^c Translational Medicine Center of Northern China   (China)

^d The University Key Laboratory of Drug Research of Heilongjiang Province   (China)

^e Medical Science Institute of Hei Longjiang Province   (China)

Author keywords

Apoptosis; Diabetic cardiomyopathy; IGF1; MicroRNA

Indexed keywords

GLUCOSE; MICRORNA; MICRORNA 483 3P; SOMATOMEDIN C; STREPTOZOCIN; UNCLASSIFIED DRUG; MIRN483 MICRORNA, MOUSE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CARDIAC MUSCLE CELL; DIABETIC CARDIOMYOPATHY; DISEASE EXACERBATION; DOWN REGULATION; EMBRYO; GENE OVEREXPRESSION; GENE REPRESSION; HEART CELL CULTURE; HYPERGLYCEMIA; IN VITRO STUDY; IN VIVO STUDY; MOUSE; NONHUMAN; PRIORITY JOURNAL; RAT; STREPTOZOTOCIN-INDUCED DIABETES MELLITUS; TRANSGENIC MOUSE; UPREGULATION; ANIMAL; C57BL MOUSE; CELL LINE; EXPERIMENTAL DIABETES MELLITUS; GENETICS; PATHOLOGY;

ANIMALS; APOPTOSIS; CELL LINE; DIABETES MELLITUS, EXPERIMENTAL; HYPERGLYCEMIA; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MICRORNAS; MYOCYTES, CARDIAC; RATS; STREPTOZOCIN;

EID: 84977663515     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2016.06.051     Document Type: Article

References (32)

1. [1] Baseler, W., Thapa, D., Jagannathan, R., et al. miR-141 as a regulator of the mitochondrial phosphate carrier (Slc25a3) in the type 1 diabetic heart. Am. J. Physiol. Cell Physiol. 303:12 (2012), C1244–C1251.
2. [2] Yu, W., Zha, W., Guo, S., et al. FLOS puerariae extract prevents myocardial apoptosis via attenuation oxidative stress in streptozotocin-induced diabetic MICE. PLOS One., 9(5), 2014 e98044.
3. [3] Abel, E.S., Diabetic cardiomyopathy revisited. Circulation. 115:25 (2007), 3213–3223.
4. [4] Li, X., Du, N., Zhang, Q., et al. MicroRNA-30d regulates cardiomyocyte pyroptosis by directly targeting foxo3a in diabetic cardiomyopathy. Cell Death Dis., 5(1), 2014 ee147-e1479.
5. [5] Control T D, Complications Trial Research Group, The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N. Engl. J. Med. 329:1 (1993), 977–986.
6. [6] Deedwania, P., Kosiborod, M., Barrett, E., et al. Hyperglycemia and acute coronary syndrome: a scientific statement from the American heart association diabetes committee of the council on nutrition, physical activity, and metabolism. Anesthesiology 109:1 (2008), 14–24.
7. [7] Wang, J., Wang, H., Hao, P., et al. Inhibition of aldehydedehydrogenase 2 by oxidative stress is associated with cardiac dysfunction in diabetic rats. Mol. Med. 17:3/4 (2011), 172–179.
8. [8] Ho, F.M., Liu, S-h, Liau, C.S., et al. High glucoseinduced apoptosis in human endothelial cells is mediated by sequential activations of c-Jun NH(2)-terminal kinase and caspase-3. Circulation 101:22 (2000), 2618–2624.
9. [9] Cai, L., Wang, Y., Zhou, G., et al. Attenuation by metallothionein of early cardiac cell death via suppression of mitochondrial[J]. J. Am. Coll. Cardiol. 48:8 (2006), 1688–1697.
10. [10] Fiordaliso, F., Leri, A., Cesselli, D., et al. Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death. Diabetes 50:10 (2001), 2363–2375.
11. [11] Fiordaliso, F., Bianchi, R., Staszewsky, L., et al. Antioxidant treatment attenuates hyperglycemia-induced cardiomyocyte death in rats. J. Mol. Cell Cardiol. 37:5 (2004), 959–968.
12. [12] Cai, L., Li, W., Wang, G., et al. Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathway. Diabetes 51:6 (2002), 1938–1948.
13. [13] Ying Li, Y.A., Tian-qing, Peng, Calpain activation contributes to hyperglycaemia-induced apoptosis in cardiomyocytes. Cardiovasc. Res. 84:1 (2009), 100–110.
14. [14] Qiao, Y., Ma, N., Wang, X., et al. MiR-483-5p controls angiogenesis in vitro and targets serum response factor. FEBS Lett. 585:19 (2011), 3095–3100.
15. [15] Pandey, A.K., Agarwal, P., Kaur, K., et al. MicroRNAs in diabetes: tiny players in big disease. Cell Physiol. Biochem. 23:4/6 (2009), 221–232.
16. [16] Em Erson, A.P., MicroRNAs in development and disease. Clin. Genet. 74:4 (2008), 296–306.
17. [17] Kantharidis, P., Wang, B., Carew, R.M., et al. Diabetes complications: the microRNA perspective. Diabetes 60:7 (2011), 1832–1837.
18. [18] Thum, T., Gross, C., Fiedler, J., et al. MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts. Nature 456:7224 (2008), 980–984.
19. [19] Feng, B., Chen, S., George, B., et al. miR133a regulates cardiomyocyte hypertrophy in diabetes. Diabetes Metab. Res. Rev. 26:1 (2000), 40–49.
20. [20] Shan, Z., Lin, Q-x, Deng, C-y, et al. miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes. FEBS Lett. 584:16 (2010), 3592–3600.
21. [21] Yu, X.Y., Song, Y.H., Geng, Y.J., et al. Glucose induces apoptosis of cardiomyocytes via microRNA-1 and IGF-1. Biochem. Biophys. Res. Commun. 376:3 (2008), 548–552.
22. [22] Landgraf, P., Rusu, M., Sheridan, R., et al. A mammalian microRNA expression Atlas based on small RNA library sequencing. Cell 129:7 (2007), 1401–1414.
23. [23] Li, F., Ma, N., Zhao, R., et al. Overexpression of miR-483-5p/3p cooperate to inhibit mouse liver fibrosis by suppressing the TGF-β stimulated HSCs in transgenic mice. J. Cell Mol. Med. 18:6 (2014), 744–760.
24. [24] Kemp, J., Unal, H., Desnoyer, R., et al. Angiotensin II-regulated microRNA 483-3p directly targets multiple components of the renin-angiotensin system. J. Mol. Cell Cardiol. 75 (2014), 25–39.
25. [25] Morley-Smith, A., Mills, A., Jacobs, S., et al. Circulating microRNAs for predicting and monitoring response to mechanical circulatory support from a left ventricular assist device. Eur. J. Heart Fail. 16:8 (2014), 871–879.
26. [26] Kotlyar, A.A., Vered, Z., Goldberg, I., et al. Insulin-like growth factor I and II preserve myocardial structure in postinfarct swine. Heart 86:6 (2001), 693–700.
27. [27] Vogt, A.M., Htun, P., Kluge, A., et al. Insulin-like growth factor-II delays myocardial infarction in experimental coronary artery occlusion. Cardiovasc Res. 33:2 (1997), 469–477.
28. [28] Gu, T., Horová, E., Möllsten, A., et al. IGF2BP2 and IGF2 genetic effects in diabetes and diabetic nephropathy. J. Diabetes Complicat. 26:5 (2012), 393–398.
29. [29] Morales, M., Gálvez, A., Eltit, J.M., et al. IGF-1 regulates apoptosis of cardiac myocyte induced by osmotic-stress. Biochem. Biophys. Res. Commun., 270(3), 2000 135.-1029.
30. [30] Lee, R.C., Feinbaum, R.L., Ambros, V., The C. elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14. Cell 75:5 (1993), 843–854.
31. [31] Huang, Y., Harrison, M.R., Osorio, A., et al. IGF signaling is required for cardiomyocyte proliferation during zebrafish heart development and regeneration. PLOS One., 26(6), 2013, 67266.
32. [32] Zou Mh, X.Z., Regulation of interplay between autophagy and apoptosis in the diabetic heart: new role of AMPK. Autophagy 9:4 (2013), 624–625.