MiR-19a Affects Hepatocyte Autophagy via Regulating lncRNA NBR2 and AMPK/PPARα in D-GalN/Lipopolysaccharide-Stimulated Hepatocytes.

This study aims to evaluate the potential involvement and regulatory mechanism of miR-19a in hepatocytes autophagy of acute liver failure (ALF). The in vitro hepatocytes injury model of primary hepatocyte and hepatocytes line HL-7702 was established by D-galactosamine (D-GalN) and lipopolysaccharide (LPS) co-treatment. Relative expression level of miR-19a and NBR2 was determined by qRT-PCR. Protein expression of AMPK/PPARα and autophagy-related gene was determined by Western blot. In hepatic tissue of 20 ALF patients and D-GalN/LPS-stimulated hepatocytes, miR-19a was upregulated and NBR2 was downregulated. D-GalN/LPS stimulation caused the inactivation of AMPK/PPARα signaling and the decrease of autophagy-related LC3-II/LC3-I ratio and beclin-1 expression in hepatocytes. The expression of both AMPK/PPARα and NBR2 were negatively controlled by miR-19a overexpression or knockdown. Moreover, both NBR2 and PPARα were targeted regulated by miR-19a according to luciferase reporter assay. In D-GalN/LPS-stimulated hepatocytes, AMPK activation promoted PPARα expression. AMPK inactivation inhibited the pro-autophagy effect of miR-19a and caused the decrease of LC3-II/LC3-I ratio and beclin-1 expression. PPARα activation abrogated the anti-autophagy effect of miR-19a mimic and caused the increase of LC3-II/LC3-I ratio and beclin-1 expression. NBR2 knockdown reversed the anti-autophagy impact of miR-19a inhibitor and caused the decrease of LC3-II/LC3-I ratio and beclin-1 expression. In summary, our data suggested that miR-19a negatively controlled the autophagy of hepatocytes attenuated in D-GalN/LPS-stimulated hepatocytes via regulating NBR2 and AMPK/PPARα signaling. J. Cell. Biochem. 119: 358-365, 2018. © 2017 Wiley Periodicals, Inc.

Quality of life in adolescent patients with idiopathic scoliosis after brace treatment: A meta-analysis.

BACKGROUND: Whether brace-treated adolescents with idiopathic scoliosis (AIS) have improved quality of life (QoL) is still unknown. Thus, we conducted a meta-analysis to compare the QoL of brace-treated AIS patients with untreated AIS patients. The pain, self-image/appearance, mental health, function/activity, satisfaction with management, total score without satisfaction, and total score of patients were used to measure the QoL after the intervention. METHODS: Multiple electronic databases including PubMed, Web of Science, and Embase were searched for all years up to June 30, 2016. Articles in English that used the Scoliosis Research Society-22 (SRS-22) or a modified version of the SRS-22 questionnaire to evaluate the QoL differences between brace-treated AIS patients and untreated AIS patients were included in the meta-analysis. The Newcastle-Ottawa Scale was used in the quality of literature evaluation. The pooled standardized mean difference (SMD) with its corresponding 95% confidence interval (CI) for each parameter was computed. Egger test and Begg test were used to test for publication bias. RESULTS: The SRS-22 or a modified SRS-22 questionnaire was used to evaluate the QoL after surgery. There was no significant difference in pain (SMD = 0.123, 95% CI: -0.101 to 0.347, P = .282), self-image/appearance (SMD = 0.108, 95% CI: -0.116 to 0.332, P = .334), mental health (SMD = 0.031, 95% CI: -0.130 to 0.201, P = .365), function/activity (SMD = 0.202, 95% CI: -0.022 to 0.425, P = .077), and total score without satisfaction (SMD = 0.123, 95% CI: -0.232 to 0.478, P = .497) between the untreated (observation) and brace-treated AIS patients, whereas a significant difference was observed in satisfaction with management (SMD = 0.393, 95% CI: 0.127-0.659, P = .004) and total score (SMD = 0.312, 95% CI: 0.054-0.571, P = .018) between the 2 groups. CONCLUSION: Our meta-analysis indicated that brace-treated AIS patients had a higher QoL. However, further analysis could not be performed because of insufficient data, such that we were unable to make subgroup analysis of QoL for different types of AIS and the therapeutic methods chosen by brace-treated AIS patients.

Regulation of the oncogenic function of distal-less 4 by microRNA-122 in hepatocellular carcinoma.

Distal-less 4 (DLX4) is a member of the DLX family of homeobox genes. Recent reports have suggested that abnormal expression of DLX4 is present in several types of human tumors, including breast cancer, leukemia and colon cancer. However, the function and the mechanistic regulation of DLX4 in hepatocellular carcinoma (HCC) are elusive. In the present study, a proportion of hepatocellular carcinomas were identified to exhibit upregulated DLX4 expression. This study proposed that the overexpression of DLX4 is associated with the downregulation of miR-122, an underexpressed miRNA in human HCC. Functional studies have demonstrated that the downregulation of DLX4 in hepatocellular carcinoma cell lines is regulated by miR-122 through binding to its 3'UTR. Furthermore, a DLX4 overexpression vector lacking the 3'UTR was shown to abolish miR-122-induced inhibition of proliferation in the HCC cell line Hep3B. These results gave new insight into the mechanism of the miR-122/DLX4 axis in HCC.