Xuzhou Medical College

About: Xuzhou Medical College is a education organization based out in Xuzhou, China. It is known for research contribution in the topics: Cancer & Cell growth. The organization has 12721 authors who have published 7802 publications receiving 102970 citations.

MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells.

Abstract: Background/Aims: Glial cell line-derived neurotrophic factor (GDNF) is an important factor promoting invasive glioma growth. This study was performed to reveal a unique mechanism of glioma cell proliferation and migration. Methods: Human U251 glioma cells were used to screen the optimal GDNF concentration and treatment time to stimulate proliferation and migration. MicroRNA (MiRNA) expression profiles were detected by microarray and confirmed by real-time polymerase chain reaction (PCR). The target genes of differentially expressed miRNAs were predicted by miRWalk, and those targeted by multiple miRNAs were screened with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. A regulatory miRNA network was constructed using ingenuity pathway analysis (IPA). Target gene expression of differentially expressed miRNAs was examined by real-time PCR or mRNA microarray. Results: The results show that 50 ng/mL GDNF for 24 h significantly promotes U251 glioma cell proliferation and migration (P < 0.05). Seven miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-629-5p, hsa-miR-3609, hsa-miR-183-5p, and hsa-miR-487b-3p) were significantly up-regulated after GDNF treatment (P < 0.05). These miRNAs are primarily involved in signal transduction, cell adhesion and cell cycle through mitogen-activated protein kinase (MAPK) signaling, focal adhesion and glioma signal pathways. Five of these miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-183-5p, and hsa-miR-487b-3p) co-regulate TP53 and Akt. mRNA expression levels of four genes co-targeted by two or more up-regulated miRNAs were significantly decreased after GDNF treatment (P < 0.05). Conclusion: GDNF treatment of U251 glioma cells significantly increased the expression of seven miRNAs involved in cell adhesion and the cell cycle.

Therapeutic Hypothermia Enhances Cold-Inducible RNA-Binding Protein Expression and Inhibits Mitochondrial Apoptosis in a Rat Model of Cardiac Arrest.

Abstract: Therapeutic hypothermia is well known for its protective effect against brain injury after cardiac arrest, but the exact mechanism remains unclear. Cold-inducible RNA-binding protein (CIRP), a member of cold shock protein, enables mammalian cells to withstand decreased temperature by regulating gene translation. However, the role of CIRP in global cerebral ischemia after therapeutic hypothermia has not been clearly elucidated. In the present study, rats resuscitated from 4 min of cardiac arrest were separately treated with therapeutic hypothermia (immediately after return of spontaneous circulation (ROSC); targeted temperature at 33 °C) and therapeutic normothermia (targeted temperature at 36.8 °C) for 6 h. The hippocampus was harvested at 0 h (baseline), 6 h, 12 h, 1 day, 3 days, and 7 days after ROSC. The expression of CIRP messenger RNA (mRNA) was assessed by real-time PCR. CIRP and mitochondrial apoptosis-associated proteins were tested by Western blot. The histological changes and neurological function were respectively evaluated by hematoxylin-eosin staining and neurological deficit score (NDS). Compared with baseline, rats resuscitated from cardiac arrest showed increased expression of CIRP, Bax, Caspase 9, and Caspase 3 and decreased expression of Bcl-2 in hippocampus (P < 0.05). However, therapeutic hypothermia after ROSC alleviated the alterations of Bax, Caspase 9, Caspase 3, and Bcl-2, while further increased the hippocampal expression of CIRP mRNA and protein, when compared with the normothermia rats (P < 0.05). In addition, compared with the therapeutic normothermia rats, histopathological damage in CA1 zone and NDS were respectively decreased and increased in the hypothermia rats (P < 0.05). Our findings suggest that 32 °C therapeutic hypothermia exerts an important neuroprotective effects by up-regulating CIRP expression and inhibiting mitochondrial apoptosis factor production in the cardiac arrest rat model.

Efficacy of orlistat in non-alcoholic fatty liver disease: A systematic review and meta-analysis.

Abstract: In the present meta-analysis, the efficacy and safety of orlistat in the treatment of non-alcoholic fatty liver (NAFLD) and non-alcoholic steatohepatitis (NASH) were evaluated. PubMed, Embase, the Cochrane Library, Web of Science, and Wan Fang data were searched for controlled trials of orlistat in patients with NAFLD or NASH, published before August 2017. Three randomized controlled trials and four single-arm trials were included. The involved participants with NAFLD or NASH (330 patients) were analyzed for clinical outcomes including alteration in hepatic histological variables and biomarkers of liver function. Improvements were observed in levels of alanine aminotransferase [standard mean difference (SMD)=-1.41; P=0.01], aspartate aminotransferase (SMD=-2.06; P=0.0005), γ-glutamyl transpeptidase (SMD=-1.91; P=0.05), glucose [mean difference (MD)=-0.51; P=0.01], triglycerides (MD=-0.93; P=0.01), homeostasis model assessment of insulin resistance index (MD=-1.05; P=0.04) and body mass index (MD=-1.97; P=0.02), but not in liver fibrosis score (SMD=-0.14; P=0.71). On sub-analyses of the different patient groups, no significant differences were observed in patients with NASH. Taken together, these findings demonstrate that orlistat could serve as a therapeutic drug to improve biochemical indicators of liver damage, but not as first-choice drug for the management of NAFLD or NASH; thus suggesting a novel palliative drug only for the treatment of NAFLD.

Sirtuin 1 alleviates diabetic neuropathic pain by regulating synaptic plasticity of spinal dorsal horn neurons

Abstract: Accumulating evidence has demonstrated that the enhanced synaptic plasticity of nociceptive interneurons in the spinal dorsal horn is the basis of central sensitization in neuropathic pain. Our previous results demonstrated that sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, alleviates neuropathic pain in type 2 diabetes mellitus rats. SIRT1 has also been reported to regulate synaptic plasticity in different brain neurons. However, the role of SIRT1 in synaptic plasticity of spinal dorsal horn neurons remains unknown. In this study, we found that in the spinal dorsal horn of diabetic neuropathic pain (DNP) rats and db/db mice, decreased SIRT1 expression was accompanied by enhanced structural synaptic plasticity. The levels of postsynaptic density protein 95 (PSD-95), growth-associated protein 43 (GAP43), and synaptophysin increased in the spinal dorsal horn of DNP rats and db/db mice and in high glucose-cultured primary spinal neurons. Upregulation of spinal SIRT1 by SIRT1 activator SRT1720 relieved pain behavior, inhibited the enhanced structural synaptic plasticity in rats and db/db mice with DNP, and decreased the levels of synapse-associated proteins in DNP rats, db/db mice, and high glucose-cultured spinal neurons. SIRT1-shRNA induced pain behavior and enhanced structural synaptic plasticity in normal rats and increased synapse-associated proteins levels in normal rats and spinal neurons. Intrathecal injection of AAV-Cre-EGFP into SIRT1 mice also induced pain behavior and enhanced synaptic plasticity of the spinal dorsal horn neurons. These results suggest that SIRT1 plays an important role in the progression of DNP by regulating synaptic plasticity of spinal dorsal horn neurons.

Effects of SEMA3G on migration and invasion of glioma cells.

Abstract: Glioblastoma multiforme is the most aggressive type of brain tumor with a strong ability to invade and migrate into surrounding normal brain tissues, leading to high tumor recurrence and mortality. Most of class-3 semaphorins, especially SEMA3A, SEMA3B and SEMA3F, have been reported to have strong tumor inhibition ability, but the role of SEMA3G in tumor biology is largely unknown. We report here that SEMA3G possesses anti-migration and anti-invasion ability. To determine the potential effects of SEMA3G on migratory and invasive ability, we generated stable SEMA3G expression U251MG cells. We found that stably overexpressed SEMA3G inhibited the migratory and invasive behavior of U251MG cells. In addition, treatment with SEMA3G conditioned media also decreased the migratory and invasive ability of parental U251MG cells. Furthermore, SEMA3G also inhibited the activity of MMP2, an index of tumor invasion ability. Thus, our results suggest that SEMA3G inhibited tumor cell migration and invasion, which may be obtained through cell autonomous or paracrine mechanisms, and SEMA3G is a potential target for antitumor migration and invasion.