MicroRNA-130b inhibits cerebral ischemia/reperfusion induced cell apoptosis via regulation of IRF1.

OBJECTIVE: Cerebral ischemia/reperfusion (CIR) frequently causes serious disabilities and correlates with certain neurological processes. Some studies have shown that microRNAs (miRNAs) exert a neuroprotective effect by modulating the inflammatory process in CIR. However, the biofunction and the mechanism of miR-130b in CIR need to be fully elucidated. MATERIALS AND METHODS: An oxygen-glucose deprivation/reperfusion (OGD/R) model was constructed using SH-SY5Y cell line to analyze the function of miR-130b in CIR. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to examine the expression levels of miR-130b and IRF1. Western blot was performed to detect the protein levels of IRF1, Bax, and Bcl-2. Cell viability was determined using MTT (3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assays. Dual-Luciferase reporter assay was conducted to confirm the target gene of miR-130b. RESULTS: In this study, we found that miR-130b level was prominently decreased after treatment with OGD/R. Through gain and loss assays, we concluded that miR-130b restoration promoted cell proliferation and inhibited cell apoptosis in OGD/R-treated cells. Moreover, we also identified IRF1 as an important target of miR-130b. Additionally, IRF1 knockdown remarkably abrogated the protection mediated by miR-130b against the injuries in OGD/R-treated cells. CONCLUSIONS: Taken together, our results suggested that miR-130b facilitated cell viability and suppressed cell apoptosis of CIR via negatively regulating of IRF1.

LncRNA XIST regulates cell proliferation, migration and invasion of glioblastoma via regulating miR-448 and ROCK1.

Long non-coding ribonucleic acids (lncRNAs) have been recognized as markers in several cancers and play important roles in glioblastoma (GBM). But the role of lncRNA X inactive-specific transcript (XIST) in GBM and its possible mechanisms are rarely studied in depth. This study was conducted to explore the detailed roles of XIST in cell proliferation, migration, and invasion of GBM. Expressions of XIST, miR-448, and ρ associated coiled coil containing protein kinase 1 (ROCK1) were detected by qRT-PCR or Western blot in A172 and U251 cells. The interactions among XIST, miR-448 and ROCK1 were verified through luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell Counting Kit-8 (CCK-8) assay and Transwell assay were introduced to detect how XIST knockdown, miR-448 overexpression, or along with ROCK1 overexpression affect cellular malignancy of GBM cells. XIST and ROCK1 were up-regulated while miR-448 expression was decreased in GBM cells. XIST knockdown or miR-448 overexpression could dramatically inhibit GBM cell proliferation, migration, and invasion. Moreover, XIST negatively regulated miR-448 expression through the function as competing endogenous RNA (ceRNA), thus leading to the up-regulation of ROCK1, one miR-448 target gene. Moreover, ROCK1 overexpression could reverse the suppression of XIST knockdown or miR-448 upregulation on cellular malignancy. In brief, the effects of XIST may promote cellular malignancy of GBM through miR-448/ROCK1 axis, which will provide new understanding of GBM pathogenesis and progression.

Effect of MWCNTs on Gastric Emptying in Mice.

After making model of gastric functional disorder (FD), part of model mice were injected intravenously (i.v.) with oxide multi-walled carbon nanotubes (oMWCNTs) to investigate effect of carbon nanotubes on gastric emptying. The results showed that NO content in stomach, compared with model group, was decreased significantly and close to normal level post-injection with oMWCNTs (500 and 800 µg/mouse). In contrast to FD or normal groups, the content of acetylcholine (Ach) in stomach was increased obviously in injection group with 500 or 800 µg/mouse of oMWCNTs. The kinetic curve of emptying was fitted to calculate gastric motility factor k; the results showed that the k of injection group was much higher than FD and normal. In other words, the gastric motility of FD mice was enhanced via injection with oMWCNTs. In certain dosage, oMWCNTs could improve gastric emptying and motility.