Erratum: Involvement of up-regulation of miR-210 in a rat epilepsy model [Corrigendum].
Ontology highlight
ABSTRACT:
SUBMITTER:
PROVIDER: S-EPMC5536313 | biostudies-other | 2017
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Objective: To investigate the potential biomarkers for venous metastasis of hepatocellular carcinoma (HCC), and briefly discuss their target genes and the signaling pathways they are involved in. Materials and Method: The dataset GSE6857 was downloaded from GEO. Significantly differentially expressed miRNAs were identified using the R package "limma," After that, the survival analysis was conducted to discover the significance of these up-regulated miRNAs for the prognosis of HCC patients. Additionally, miRNAs which were up-regulated in venous metastasis positive HCC tissues and were significant for the prognosis of HCC patients were further verified in clinical samples using RT-qPCR. The miRNAs were then analyzed for their correlations with clinical characteristics including survival time, AFP level, pathological grade, TNM stage, tumor stage, lymph-node metastasis, distant metastasis, child-pugh score, vascular invasion, liver fibrosis and race using 375 HCC samples downloaded from the TCGA database. The target genes of these miRNAs were obtained using a miRNA target gene prediction database, and their functions were analyzed using the online tool DAVID. Results: 15 miRNAs were differentially expressed in samples with venous metastasis, among which 7 were up-regulated in venous metastasis positive HCC samples. As one of the up-regulated miRNAs, hsa-miR-210 was identified as an independent prognostic factor for HCC. Using RT-qPCR, it was evident that hsa-miR-210 expression was significantly higher in venous metastasis positive HCC samples (p = 0.0036). Further analysis indicated that hsa-miR-210 was positively associated with AFP level, pathological grade, TNM stage, tumor stage and vascular invasion. A total of 168 hsa-miR-210 target genes, which are mainly related to tumor metastasis and tumor signaling pathways, were also predicted in this study. Conclusion: hsa-miR-210 might promote vascular invasion of HCC cells and could be used as a prognostic biomarker.
| S-EPMC6287006 | biostudies-literature
Project description:[This corrects the article DOI: 10.1107/S1600536807044108.].
| S-EPMC8025866 | biostudies-literature
Project description:Consideration of a previous unrecognized twinning of the original investigated crystal of the title compound [Kia et al. (2009 ?). Acta Cryst. E65, o301] led to improved reliability factors and to a slightly higher precision for all geometric parameters. The crystal under investigation was twinned by pseudo-merohedry with [100, 00, 00]?as the twin matrix and a refined twin domain fraction of 0.9610?(5):0.0390?(5). The results of the new crystal structure refinement are given here.[This corrects the article DOI: 10.1107/S1600536809001068.].
| S-EPMC2969655 | biostudies-literature
Project description:Ex vivo culture has been proposed as a means to augment and repair autologous cells in patients with chronic diseases, but the mechanisms governing improvement in cell function are not well understood. Although microRNAs (miRs) are increasingly appreciated as key regulators of cellular function, a role for these factors in CD34+ cell-mediated angiogenesis has not been elucidated. Vascular endothelial growth factor (VEGF) was previously shown to induce expression of certain miRs associated with angiogenesis in endothelial cells and promote survival and number of vascular colony forming units of haematopoietic stem cells (HSCs). We sought to evaluate the role of VEGF in expansion and angiogenic function of CD34+ cells and to identify specific miRs associated with angiogenic properties of expanded cells. Umbilical cord blood CD34+ cells were effectively expanded (18- to 22-fold) in culture medium containing stem cell factor (SCF), Flt-3 ligand (Flt-3), thrombopoietin (TPO) and interleukin-6 (IL-6) with (postEX/+VEGF) and without VEGF (postEX/noVEGF). Tube formation in matrigel assay and tissue perfusion/capillary density in mice ischaemic hindlimb were significantly improved by postEX/+VEGF cells compared with fresh CD34+ and postEX/noVEGF cells. MiR-210 expression was significantly up-regulated in postEX/+VEGF cells. MiR-210 inhibitor abrogated and 210 mimic recapitulated the pro-angiogenic effects by treatment of postEX/+VEGF and postEX/noVEGF cells respectively. Collectively, these observations highlight a critical role for VEGF in enhancing the angiogenic property of expanded cells, and identify miR-210 as a potential therapeutic target to enhance CD34+ stem cell function for the treatment of ischaemic vascular disease.
| S-EPMC3823435 | biostudies-literature
Project description:An error in the original formulation of the title compound in the paper by Sadiq-ur-Rehman, Sherzaman, Ali, Shahzadi & Helliwell [Acta Cryst. (2007), E63, m2329] is corrected.The title compound in the paper by Sadiq-ur-Rehman, Sherzaman, Ali, Shahzadi & Helliwell [Acta Cryst. (2007), E63, m2329] was an unexpected product which seemed to have nitrate coordinated to three Sn atoms. However, it was noticed that the charges do not balance and that it is most likely that the nitrate is in fact a carbonate. Regrettably, there is no material to carry out microanalysis, but a plausible mechanism has been suggested to explain the unexpected formation of the product. Trimethyl-tin chloride will react with methanol in the presence of a base (4-hydroxy-piperidine) to give trimethyl-tin methoxide, which will rapidly hydrolyze in air to give the hydroxide. Both the methoxide and the hydroxide will react with atmospheric CO(2) to give the carbonate (Bloodworth et al., 1967 ?; Blunden et al., 1984 ?; Sato, 1967 ?). Me(3)SnCl + MeOH + base ? Me(3)SnOMe + base·HCl Me(3)SnOMe + H(2)O ? Me(3)SnOH + MeOH Me(3)SnOH + CO(2) ? Me(3)SnOCO(2)HMe(3)SnOCO(2)H + Me(3)SnOMe ? Me(3)SnOCO(2)SnMe(3) + MeOH. The carbonate then forms a coordination copolymer with trimethyl-tin chloride. The name of the title compound is corrected to poly[?(3)-carbonato-?(3)-chlorido-nona-methyl-tri-tin(IV)], [Sn(3)(CH(3))(9)(CO(3))Cl] (M(r) = 586.84).[This corrects the article DOI: 10.1107/S1600536808017091.].
| S-EPMC2961754 | biostudies-literature
Project description:[This corrects the article on p. 359 in vol. 8, PMID: 26604805.].
| S-EPMC4822793 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-02-13 | GSE27268 | GEO
Project description:Inflammation events have been found to aggravate brain injury and blood-brain barrier (BBB) damage following subarachnoid hemorrhage (SAH). This study probed the role and mechanism of a novel circRNA, circARF3, in regulating the BBB injury in SAH rats and hypoxia-induced vascular endothelial cell (VEC) injury in vitro. Levels of circARF3 and miR-31-5p were monitored by RT-PCR. The expression of inflammatory factors IL-1β and TNF-α was verified by ELISA. In vivo SAH model was constructed in Sprague Dawley (SD) rats. The BBB integrity and cerebral edema, as well as the neurological functions of the rats were evaluated. The apoptotic neurons and microglia in brain lesions were examined by immunohistochemistry (IHC). The MyD88/NF-κB pathway was tested by Western blot. Furthermore, gain-of functional assay were constructed to explore the effects of circARF3 and miR-31-5p in primary cultured brain microvascular endothelial cell (BMEC) injury and microglial inflammation induced by oxygen and glucose deprivation (OGD). circARF3 was significantly down-regulated in plasma and CSF in SAH patients with higher Fisher stages. In the SAH rat model, overexpressing circARF3 improved BBB integrity and neurological score, decreased neuronal apoptosis and microglial activation in ipsilateral basal cortex, with declined miR-31-5p expression and MyD88-NF-κB activation. In vitro, overexpressing circARF3 attenuated OGD-mediated integrity destruction of BMECs and microglial induced neuroinflammation, while overexpressing miR-31-5p had opposite effects. Mechanistically, circARF3 sponged miR-31-5p as an endogenous competitive RNA and dampens its expression, thus inactivating MyD88-NF-κB pathway. CircARF3 attenuates BBB destruction in SAH rats by regulating the miR-31-5p-activated MyD88-NF-κB pathway.
| S-EPMC8457610 | biostudies-literature
Project description:As miR-210 expression is correlated to poor prognosis both in estrogen-positive and in estrogen-negative breast cancer (BC) patients, we aimed to investigate the biological processes regulated by miR-210 and which may elucidate its function in the aggressive phenotype of high grade breast cancer. We performed in silico functional analyses of the genes deregulated upon miR-210 overexpression in MCF7 BC cell line and upon miR-210 repression in MDA-MB-231 BC cell line using lentiviral transduction. Gene expression profiling analysis of these cells revealed the deregulation of genes involved in several biological pathways including cell adhesion, extracellular structure organization, epithelial cell proliferation, cell division, cell cycle and immune response. MCF-7 cells overexpressing miR-210 (or control) and MDA-MB-231 cells in which miR-210 (or control) is repressed were used for RNA extraction and hybridization on Affymetrix microarrays.
| S-ECPF-GEOD-25162 | biostudies-other
Project description:Neither the molecular basis of the pathologic tendency of neuronal circuits to generate spontaneous seizures (epileptogenicity) nor anti-epileptogenic mechanisms that maintain a seizure-free state are well understood. Here, we performed transcriptomic analysis in the intrahippocampal kainate model of temporal lobe epilepsy in rats using both Agilent and Codelink microarray platforms to characterize the epileptic processes. The experimental design allowed subtraction of the confounding effects of the lesion, identification of expression changes associated with epileptogenicity, and genes upregulated by seizures with potential homeostatic anti-epileptogenic effects. Using differential expression analysis, we identified several hundred expression changes in chronic epilepsy, including candidate genes associated with epileptogenicity such as Bdnf and Kcnj13. To analyze these data from a systems perspective, we applied weighted gene co-expression network analysis (WGCNA) to identify groups of co-expressed genes (modules) and their central (hub) genes. One such module contained genes upregulated in the epileptogenic region, including multiple epileptogenicity candidate genes, and was found to be involved the protection of glial cells against oxidative stress, implicating glial oxidative stress in epileptogenicity. Another distinct module corresponded to the effects of chronic seizures and represented changes in neuronal synaptic vesicle trafficking. We found that the network structure and connectivity of one hub gene, Sv2a, showed significant changes between normal and epileptogenic tissue, becoming more highly connected in epileptic brain. Since Sv2a is a target of the antiepileptic levetiracetam, this module may be important in controlling seizure activity. Bioinformatic analysis of this module also revealed a potential mechanism for the observed transcriptional changes via generation of longer alternatively polyadenlyated transcripts through the upregulation of the RNA binding protein HuD. In summary, combining conventional statistical methods and network analysis allowed us to interpret the differentially regulated genes from a systems perspective, yielding new insight into several biological pathways underlying homeostatic anti-epileptogenic effects and epileptogenicity.
2011-02-13 | GSE27166 | GEO