IntroductionThe purpose of this study was to investigate the expression of Wnt and Notch signaling pathway-related genes in inflammatory bowel disease (IBD) treated with mesenchymal stem cell transplantation (MSCT).MethodsTNBS (2,4,6-trinitrobenzene sulfonic acid) was used to establish IBD in a rat model. Mesenchymal stem cells (MSCs) were transplanted via tail vein transfusion. Saline water was used in a control group. The expression of Wnt and Notch main signaling molecules was screened by gene chips and verified by quantitative reverse transcription-polymerase chain reaction in the IBD rat model on day 14 and day 28 after transplantation.ResultsThe IBD rat models were successfully established and MSCs were transplanted into those models. Genome-wide expression profile chips identified a total of 388 differentially expressive genes, of which 191 were upregulated and 197 were downregulated in the MSC-transplanted group in comparison with the IBD control group. Real-time quantitative polymerase chain reaction results showed that the level of Olfm4 mRNA expression in the IBD group (2.54±0.20) was significantly increased compared with the MSCT group (1.39±0.54) and the normal group (1.62±0.25) (P <0.05). The Wnt3a mRNA was more highly expressed in IBD rats (2.92±0.94) and decreased in MSCT rats (0.17±0.63, P <0.05). The expression of GSK-3β mRNA was decreased in the setting of inflammation (0.65±0.04 versus 1.00±0.01 in normal group, P <0.05) but returned to normal levels after MSCT (0.81±0.17). The expression of β-catenin was observed to increase in IBD tissues (1.76±0.44) compared with normal tissues (1.00±0.01, P <0.05), but no difference was found in the MSCT group (1.12±0.36). Wnt11 declined at 14 days and returned to normal levels at 28 days in the IBD group; in comparison, a significantly lower expression was found in MSCT rats. There were no differences in the expression of Fzd3, c-myc, TCF4, and Wnt5a in inflammation, but all of those genes declined after MSCT treatment.ConclusionsThe canonical Wnt and Notch signaling pathways are activated in IBD and may be suppressed by stem cell transplantation to differentiate into intestinal epithelium after MSCT. Moreover, the non-canonical Wnt signaling may be inhibited by canonical Wnt signaling in the setting of inflammation and may also be suppressed by MSCT.
Introduction: Stored red blood cells (RBCs) undergo storage lesions involving morphological, physiological and biochemical changes. MicroRNAs (miRNAs) have important functions in cell apoptosis and life processes. Therefore, the aim of this study was to explore potential roles of miRNAs in the damage of stored RBCs. Methods: Blood samples were collected from 13 healthy male O-type donors, and leuko-reduced RBCs were divided into fresh RBC group and 20-day storage RBC group. Results: Eight predicted miRNAs with modified expressions with an intersection ≥ 3 were found dysregulated in the 20-day storage RBC group and involved in apoptosis and senescence signaling pathway: miR-31-5p, miR-196a-5p, miR-203a, miR-654-3p and miR-769-3p were increased, while miR-96-5P, miR-150-5P and miR-197-3p were decreased. Evidence associating miR-31-5p, miR-203a, miR-654 and miR-769 to RBCs or blood in general are not available. Conclusions: Dysregulated miRNAs might represent potential biomarkers to identify storage lesions, and their detection might help to evaluate the quality of stored RBCs.
Previous studies have demonstrated that microRNAs (miRNAs/miRs) act as tumor suppressors or oncogenes during multiple processes in cancer. It has been observed that miR-27b may act as a tumor-suppressor and was significantly downregulated in a number of types of cancer. However, the functions of miR-27b in gastric cancer (GC) remain unclear. The present study aimed to investigate the functional role of miR-27b in the progression of GC. The downregulation of miR-27b in human GC plasma was confirmed using miRNA microarray and reverse transcription-quantitative polymerase chain reaction analyses. The association between circulating miR-27b expression and clinicopathological features of GC was analyzed and the results demonstrated that the level of circulating miR-27b was significantly correlated with GC differentiation. Receiver operating characteristic curve analysis identified that the plasma level of miR-27b may be a potential biomarker for differentiating patients with GC from healthy controls. In order to investigate the effect of miR-27b on GC cell behavior, miR-27b was overexpressed using miR-27b mimics, and it was observed that miR-27b was able to inhibit cell proliferation and induce apoptosis in SGC7901 cells. Previous studies have demonstrated that vascular endothelial growth factor C (VEGFC) is a target of miR-27b, and the results of the present study were consistent with these reports. Taken together, the results of the present study indicated that miR-27b may act as a potential biomarker for differentiating patients with GC from healthy controls, and serve as a tumor suppressor in GC by targeting VEGFC.
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