The antidepressant effects of protein arginine methyltransferase 2 involve neuroinflammation.

Protein arginine methyltransferase (PRMT) 2 catalyzes the methylation of arginine residues in histones. Depression is associated with histone methylation; however, more comprehensive research is needed on how PRMT2 regulates depression. The present study aimed to investigate the effects and possible mechanism(s) of PRMT2 overexpression on depression-like behavior induced by chronic unpredictable mild stress (CUMS) in rats, and whether lentivirus-mediated PRMT2 overexpression in the hippocampus suppresses depression-like behavior. Furthermore, the PRMT2 inhibitor MS023 was administered to the animals to investigate whether the antidepressant effect of PRMT2 overexpression could be reversed. Behavioral experiments were performed to detect depression-like behavior in rats. Western blotting was used to determine protein expression levels of PRMT2, histone H3R8 asymmetric dimethylation (H3R8me2a), inducible nitric oxide synthase (iNOS), and arginase 1 (Arg1) in rat hippocampal tissues. Hippocampal microglia and PRMT2 were stained using immunofluorescence techniques. Enzyme-linked immunosorbent assay was used to determine the levels of various inflammatory factors in rat hippocampal tissue. Results of analysis revealed that PRMT2 overexpression in the hippocampus exerted an antidepressant effect. PRMT2 overexpression in the hippocampus reduced the proportion of activated microglia in the hippocampus, upregulated Arg1 and H3R8me2a expression, and downregulated iNOS expression. PRMT2 overexpression in the hippocampus inhibited the release of pro-inflammatory factors and promoted the release of anti-inflammatory factors. In summary, PRMT2 overexpression in the hippocampus promoted the conversion of microglia from the M1 to M2 type, resulting in an antidepressant effect. These results suggest that PRMT2 may be a potential therapeutic target to prevent and treat depression.

circEPSTI1 promotes tumor progression and cisplatin resistance via upregulating MSH2 in cervical cancer.

CircRNAs (circRNAs) are a kind of non-coding RNAs which are extensively distributed in tissues. Previous investigations reported that circRNAs harbor indispensable roles in modulating the progress of multiple cancers. Nevertheless, the function along with the molecular mechanism of most circRNAs in cervical cancer progression was still not clear. Herein, we illustrated that circEPSTI1 is a remarkably upregulated circRNA, which we validated in tissues with cervical cancer along with cell lines. The biological role of circEPSTI1 in the advancement of cervical cancer was probed via loss-of function assessments. Silencing circEPSTI1 could diminish the proliferative capacity of the cervical cancer cells to spread. In cervical cancer cells, silencing circEPSTI1 dramatically elevated drug responsivity to cisplatin. Mechanically, RNA immuno-precipitation experiments and dual luciferase enzyme reporter experiments were conducted to reveal the molecular mechanism of circEPSTI1 in cervical cancer. In conclusion, this research premise identified the biological function of circEPSTI1-miR-370-3p-MSH2 axis in cervical cancer progression. Our result is significant for slowing the progress of and overcoming drug resistance of cervical cancer.