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

Qiao, Yu; Zhao, Yanli; Liu, Yan; Ma, Ning; Wang, Chuxuan; Zou, Jiaqi; Liu, Zhiyan; Zhou, Zhongqiu; Han, Dong; He, Jiang; Sun, Qian; Liu, Yicong; Xu, Chi; Du, Zhenhong; Huang, Hui

doi:10.1016/j.bbrc.2016.06.051

Cited by 46 publications

(37 citation statements)

References 31 publications

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“…Therefore, the reason for this difference in functionality needs further verification. Interestingly, IGF1 can be targeted by miR‐483, which had been interpreted in KGN (human ovarian granulosa cell line) proliferation (Xiang et al, ) and cardiomyocyte apoptosis (Qiao et al, ). Furthermore, miR‐483 is also involved in the regulation of different signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

Song

Dong

et al. 2018

Journal Cellular Physiology

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MicroRNAs (miRNAs) have been established to regulate skeletal muscle development in mammals. However, few studies have been conducted on the regulation of proliferation and differentiation of bovine myoblast cells by miRNAs. The aim of our study was to explore the function of miR‐483 in cell proliferation and differentiation of bovine myoblast. Here, we found that miR‐483 declined in both proliferation and differentiation stages of bovine myoblast cells. During the proliferation phase, the overexpression of miR‐483 downregulated the cell cycle–associated genes cyclin‐dependent kinase 2 (CDK2), proliferating cell nuclear antigen (PCNA) messenger RNA (mRNA), and the protein levels. At the cellular level, cell cycle, cell counting kit‐8, and 5‐ethynyl‐2´‐deoxyuridine results indicated that the overexpression of miR‐483 block cell proliferation. During differentiation, the overexpression of miR‐483 led to a decrease in the levels of the myogenic marker genes MyoD1 and MyoG mRNA and protein. Furthermore, the immunofluorescence analysis results showed that the number of MyHC‐positive myotubes was reduced. In contrast, the opposite experimental results were obtained concerning both proliferation and differentiation after the inhibition of miR‐483. Mechanistically, we demonstrated that miR‐483 target insulin‐like growth factor 1 (IGF1) and downregulated the expression of key proteins in the PI3K/AKT signaling pathway. Altogether, our findings indicate that miR‐483 acts as a negative regulator of bovine myoblast cell proliferation and differentiation.

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Section: Discussionmentioning

confidence: 99%

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

Song

Dong

et al. 2018

Journal Cellular Physiology

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“…miR-483 was initially identified in the human fetal liver (16) and is located within intron 2 of the insulin-like growth factor 2 locus (17). It serves important roles in the mechanism of many diseases, including alcoholic hepatitis (18), diabetic cardiomyopathy (19), ovarian carcinoma (20) and pancreatic cancer (21). In the present study, the effect of miR-483-3p in breast cancer was investigated and the results demonstrated that miR-483-3p was downregulated in breast cancer cell lines, especially in MCF7 cells.…”

Section: Discussionmentioning

confidence: 99%

Tumor suppressor function of miR‑483‑3p on breast cancer via targeting of the cyclin E1 gene

Huang

Jin

2018

Exp Ther Med

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microRNA (miR)-483-3p has previously been demonstrated to be a tumor suppressor in many types of cancer cells, however it is unknown whether miR-483-3p is involved in the regulation of breast cancer. Therefore, the aim of the present study was to investigate the effects of miR-483-3p on breast cancer. The results demonstrated that the expression of miR-483-3p was decreased, especially in MCF-7 cells. The results of CCK-8 assay and cell cycle analysis demonstrated that miR-483-3p significantly reduced cell proliferation and inhibited MCF-7 cells in the G1 phase from entering the S phase (P<0.01). It was also demonstrated that Cyclin E1 (CCNE1) is a target gene of miR-483-3p using bioinformatics and a dual luciferase reporter assay. miR-483-3p inhibited the expression of CCNE1, cyclin-dependent kinase 2, nuclear protein ataxia-telangiectasia (NPAT) and phosphorylated NPAT. Therefore, the results indicated that miR-483-3p functions as a tumor suppression in breast cancer and CCNE1 is its target gene. Downstream genes of CCNE1 were also repressed by miR-483-3p. Therefore, these findings suggest that miR-483-3p is a key factor in breast cancer.

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“…Among the miRNAs miR-21 [60], miR-320 [61], miR-141 [62], miR-30d [58], miR-34a [63], miR-301a [64], miR-451 [65], miR-206, miR-223 [66, 67], miR-483-3p [68], miR-216a, miR-221 [69], miR-195 [70], miR-199a-3p, miR-700, miR-142-3p, miR-24, miR-499-3p, miR-208a and miR-705 [71] have often been found to be upregulated, whereas miR-133a [72, 73], miR-150 [74], miR-29 [75], miR-144 [76], miR-378 [77], miR-499 [50], miR-143, miR-30c, miR-181a [78], miR-9 [79] , miR-23b [80], miR-1, miR-373, miR-20a and miR-220b [71], have been found to be downregulated in under diabetic conditions.…”

Section: Role Of Mirna In Diabetic Cardiomyopathymentioning

confidence: 99%

Role of microRNA in diabetic cardiomyopathy: From mechanism to intervention

Guo

Nair

2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Diabetic cardiomyopathy is a chronic and irreversible heart complication in diabetic patients, and is characterized by complex pathophysiologic events including early diastolic dysfunction, cardiac hypertrophy, ventricular dilation and systolic dysfunction, eventually resulting in heart failure. Despite these characteristics, the underlying mechanisms leading to diabetic cardiomyopathy are still elusive. Recent studies have implicated microRNA, a small and highly conserved non-coding RNA molecule, in the etiology of diabetes and its complications, suggesting a potentially novel approach for the diagnosis and treatment of diabetic cardiomyopathy. This brief review aims at capturing recent studies related to the role of microRNA in diabetic cardiomyopathy.

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

Cited by 46 publications

References 31 publications

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

Tumor suppressor function of miR‑483‑3p on breast cancer via targeting of the cyclin E1 gene

Role of microRNA in diabetic cardiomyopathy: From mechanism to intervention

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