MicroRNA-200a-3p accelerates the progression of osteoporosis by targeting glutaminase to inhibit osteogenic differentiation of bone marrow mesenchymal stem cells.
Only the miR-200a-3p level was continuously elevated under prolonged stress, suggesting roles of reduced neurogenesis, inflammatory activation, disturbed circadian rhythm, lipid metabolism, and insulin secretion in the co-existence of pain and depression.
Compared with healthy newborn rabbits, the mRNA and protein expression levels of miR-200a and IL-10 in the blood of newborn rabbits with RDS decreased significantly (p<0.05), while β-catenin increased markedly (p<0.05).
Finally, after adjusting for other important prognostic confounders, patients with high expression of miR-200a-3p, miR-30b-5p and miR-4451 had significantly high risk of overall death and death owing to HSCC and patients with a high-risk score has approximately 2-fold increased risk in overall death and death owing to HSCC compared with those with a low-risk score.
The methylation rates of miR-1247 and miR-200a were significantly higher in patients with pancreatic cancer, and biliary tract cancer than in those with benign diseases, and the methylation rate of miR-200b was significantly higher in patients with pancreatic cancer than in those with benign diseases.
These results support the involvement of selenoproteins and glucose metabolism in the control of cardiomyocytes hypertrophy by Se-specific miRNA, suggesting that miR-200a-5p inhibited the expression of stress-related selenoproteins to alter glucose transport leading to glucose metabolism disorder, eventually inducing cardiomyocytes hypertrophy.
<b>Conclusion:</b> miR-200a/200b are involved in modulating HG-induced endothelial inflammation by regulating OGT-mediated protein <i>O</i>-GlcNAcylation, suggesting the therapeutic role of miR-200a/200b on vascular complications in diabetes.
<b>Conclusion:</b> miR-200a/200b are involved in modulating HG-induced endothelial inflammation by regulating OGT-mediated protein <i>O</i>-GlcNAcylation, suggesting the therapeutic role of miR-200a/200b on vascular complications in diabetes.
Our present study provides a new insight that the modulation of miR-200a-5p and its target gene might block necroptosis in the heart, revealing a novel myocardial necrosis regulation model in heart disease.
These findings provide a novel pathological mechanism of fructose-induced redox status imbalance and suggest that the enhancement of miR-200a to control Keap1/Nrf2 pathway by polydatin is a therapeutic strategy for fructose-associated liver inflammation and lipid deposition.
This study suggests that miR-200a could induce visceral hyperalgesia by targeting the downregulation of CNR1 and SERT, aggravating or leading to the development and progression of IBS-D. MiR-200a may be a regulator of visceral hypersensitivity, which provides potential targets for the treatment of IBS-D.