miR-30c and miR-181a synergistically modulate p53?p21 pathway in diabetes induced cardiac hypertrophy

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dc.contributor.authorRaut, Satish K.
dc.contributor.authorSingh, Gurinder B.
dc.contributor.authorRastogi, Bhawna
dc.contributor.authorSaikia, Uma Nahar
dc.contributor.authorMittal, Anupam
dc.contributor.authorDogra, Nilambra
dc.contributor.authorSingh, Sandeep
dc.contributor.authorPrasad, Rishikesh
dc.contributor.authorKhullar, Madhu
dc.date.accessioned2018-07-14T01:18:57Z
dc.date.accessioned2024-08-14T07:41:19Z
dc.date.available2018-07-14T01:18:57Z
dc.date.available2024-08-14T07:41:19Z
dc.date.issued2016
dc.description.abstractp53?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.en_US
dc.identifier.citationRaut, 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/s11010-016-2729-7en_US
dc.identifier.doi10.1007/s11010-016-2729-7
dc.identifier.issn3008177
dc.identifier.urihttp://10.2.3.109/handle/32116/1395
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs11010-016-2729-7
dc.language.isoenen_US
dc.publisherSpringer New York LLCen_US
dc.subjectMicrornaen_US
dc.subjectMicrorna 181Aen_US
dc.subjectMicrorna 30Cen_US
dc.subjectProtein P21en_US
dc.subjectProtein P53en_US
dc.subjectUnclassified Drugen_US
dc.subjectCdkn1A Protein, Raten_US
dc.subjectCyclin Dependent Kinase Inhibitor 1Aen_US
dc.subjectMicrornaen_US
dc.subjectMirn181 Microrna, Raten_US
dc.subjectMirn30 Microrna, Raten_US
dc.subjectProtein P53en_US
dc.subjectAnimal Cellen_US
dc.subjectAnimal Experimenten_US
dc.subjectAnimal Modelen_US
dc.subjectAnimal Tissueen_US
dc.subjectApoptosis Cardiac Muscle Cellen_US
dc.subjectCell Sizeen_US
dc.subjectControlled Studyen_US
dc.subjectDiabetes Mellitusen_US
dc.subjectDiabetic Cardiomyopathyen_US
dc.subjectDiabetic Patienten_US
dc.subjectDisease Associationen_US
dc.subjectEnzyme Inhibitionen_US
dc.subjectGene Expressionen_US
dc.subjectHeart Ventricle Hypertrophyen_US
dc.subjectHumanen_US
dc.subjectHumen_US
dc.titlemiR-30c and miR-181a synergistically modulate p53?p21 pathway in diabetes induced cardiac hypertrophyen_US
dc.title.journalMolecular and Cellular Biochemistry
dc.typeArticleen_US

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