Raut, Satish K.Singh, Gurinder B.Rastogi, BhawnaSaikia, Uma NaharMittal, AnupamDogra, NilambraSingh, SandeepPrasad, RishikeshKhullar, Madhu2018-07-142024-08-142018-07-142024-08-142016Raut, S. K., Singh, G. B., Rastogi, B., Saikia, U. N., Mittal, A., Dogra, N., . . . Khullar, M. (2016). miR-30c and miR-181a synergistically modulate p53?p21 pathway in diabetes induced cardiac hypertrophy. Molecular and Cellular Biochemistry, 417(1-2), 191-203. doi: 10.1007/s11010-016-2729-7300817710.1007/s11010-016-2729-7http://10.2.3.109/handle/32116/1395p53?p21 pathway mediates cardiomyocyte hypertrophy and apoptosis and is upregulated in diabetic cardiomyopathy (DbCM). We investigated role of microRNAs in regulating p53?p21 pathway in high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis. miR-30c and miR-181a were identified to target p53. Cardiac expression of microRNAs was measured in diabetic patients, diabetic rats, and in HG-treated cardiomyocytes. Effect of microRNAs over-expression and inhibition on HG-induced cardiomyocyte hypertrophy and apoptosis was examined. Myocardial expression of p53 and p21 genes was increased and expression of miR-30c and miR-181a was significantly decreased in diabetic patients, DbCM rats, and in HG-treated cardiomyocytes. Luciferase assay confirmed p53 as target of miR-30c and miR-181a. Over-expression of miR-30c or miR-181a decreased expression of p53, p21, ANP, cardiomyocyte cell size, and apoptosis in HG-treated cardiomyocytes. Concurrent over-expression of these microRNAs resulted in greater decrease in cardiomyocyte hypertrophy and apoptosis, suggesting a synergistic effect of these microRNAs. Our results suggest that dysregulation of miR-30c and miR-181a may be involved in upregulation of p53?p21 pathway in DbCM. ? 2016, Springer Science+Business Media New York.enMicrornaMicrorna 181AMicrorna 30CProtein P21Protein P53Unclassified DrugCdkn1A Protein, RatCyclin Dependent Kinase Inhibitor 1AMicrornaMirn181 Microrna, RatMirn30 Microrna, RatProtein P53Animal CellAnimal ExperimentAnimal ModelAnimal TissueApoptosis Cardiac Muscle CellCell SizeControlled StudyDiabetes MellitusDiabetic CardiomyopathyDiabetic PatientDisease AssociationEnzyme InhibitionGene ExpressionHeart Ventricle HypertrophyHumanHumArticlehttps://link.springer.com/article/10.1007%2Fs11010-016-2729-7