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https://www.selleckchem.com/pharmacological_epigenetics.html Knockdown of mmu-miR-324-5p increased the levels of lncDum and myogenesis-related gene expression. Following oleate-induced lipid deposition in C2C12 myoblasts, overexpression of mmu-miR-324-5p decreased the expression of Pm20d1 while increasing the expression of mitochondrial β-oxidation and long-chain fatty acid synthesis-related genes. In conclusion, we provide evidence that miR-324-5p inhibits C2C12 myoblast differentiation and promotes intramuscular lipid deposition by targeting lncDum and Pm20d1, respectively.Meningitic Escherichia coli invasion of the host brain can lead to increased blood-brain barrier (BBB) permeability. Circular RNAs (circRNAs) are non-coding RNAs, highly abundant in the brain, that are widely involved in the pathological processes of central nervous system (CNS) disorders; however, whether circRNAs participate in the regulation of BBB permeability during E. coli meningitis remains unknown. Here, we identified a novel circRNA, circ_2858, that was significantly upregulated in human brain microvascular endothelial cells (hBMECs) upon meningitic E. coli infection. We also found that circ_2858 regulated BBB permeability in hBMECs by competitively binding miR-93-5p, thereby inducing the upregulation of vascular endothelial growth factor A and finally resulting in downregulation as well as altered distribution of tight junction proteins such as ZO-1, Occludin, and Claudin-5. These findings provide novel insights into the influence of circ_2858 on BBB permeability during the pathogenic process of E. coli meningitis, suggesting potential nucleic acid targets for future prevention and therapy of CNS infection induced by meningitic E. coli.Despite significant advances in the treatment of myocardial ischemia-reperfusion (I/R) injury, coronary circulation is a so far neglected target of cardioprotection. In this study, we investigated the molecular mechanisms underlying I/R injury to cardiac

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