The present study aimed to ascertain the potential roles and mechanisms of action of micro (mi)RNA-22 in ischemic stroke. The results indicated that miRNA-22 expression was downregulated in ischemic stroke rats model, compared with a control group. The downregulation of miRNA-22 upregulated the expression of inflammatory factors [including tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and IL-18]. It could also induce the expression of macrophage inflammatory protein (MIP-2), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) in the in vitro model. By contrast, the overexpression of miRNA-22 downregulated the expression of inflammatory factors, and suppressed the expression of MIP-2, PGE2, COX-2 and iNOS in the in vitro model. The downregulation of miRNA-22 induced the protein expression of nuclear factor (NF)-κB and phosphorylated-p38 (p-p38) mitogen-activated protein kinase (MAPK) in the in vitro model. By comparison, the overexpression of miRNA-22 suppressed the protein expression of NF-κB and p-p38 in the in vitro model. Typically, LY2228820, the p38 inhibitor (3 nM) would mitigate the pro-inflammatory effects of anti-miRNA-22 in the in vitro model. These results suggested that miRNA-22 can alleviate ischemic stroke-induced inflammation in rats model or vitro model through p38 MAPK/NF-κB pathway suppression.
Accumulating evidence has shown that miR-429 plays an important role in the development and progression of tumour. However, the role of miR-429 in glioblastoma multiforme (GBM) remains largely unknown. The present study is designed to investigate the function of miR-429 in GBM and to explore the molecular mechanism underlying its function. The expression level of miR-429 was detected in GBM tissues and cell lines by quantitative real-time polymerase chain reaction. The effect of overexpression of miR-429 on in vitro cell proliferation, apoptosis and invasion was examined. Western blot analysis was used to detect the influence of miR-429 on the expression of target gene, and Pearson analysis was used to calculate the correlation between the expression of targets gene and the miR-429 in GBM tissues. Our study shows that miR-429 is downregulated in GBM tissues compared with noncancerous tissues (P < .01). In addition, the expression of miR-429 in GBM cell lines is also significantly lower (P < .01). Enforced expression of miR-429 inhibits GBM cells proliferation, induces apoptosis and suppresses invasion and leads to the downregulation of the SOX2 protein. Moreover, the expression level of miR-429 in GBM tissues shows inverse relationship with the expression level of SOX2 protein. Our findings suggest that miR-429 represents a potential tumour-suppressive miRNA and plays an important role in GBM progression by directly targeting SOX2.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.