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Based on the gastric cancer patient database from Kaplan-Meier Plotter tools, we found that 8 of 10 genes with most significant changes in the miRNA-gene regulatory network possessed a prognostic value for survival time of gastric cancer patients. Patients with higher level of RGS1, PLEKHB2, TAX1BP3 and PSENEN in gastric cancer had a longer survival time compared with the patients with lower level of these genes. On the contrary, patients with higher level of INHBA, SNTG1, TNFRSF19 and NME3 were found associated with a shorter survival time. In conclusion, our findings provided several potential targets regarding gastric cancer, which may result in a new strategy to treat gastric cancer from a system rather than a single-gene perspective.The challenge to avoid or reduce cardiopulmonary bypass-related injuries in cardiovascular surgery remains a major issue. Remote ischemic preconditioning (RIPC) remains a promising strategy whose clinical applications appear to be significantly more realistic and extensive as compared with other conservative or surgical strategies. However, considering its underlying mechanism(s) are still unclear, novel ideas and methods must be explored to enhance its potential in clinical applications. Long noncoding RNAs (LncRNAs) are a kind of RNAs that have been implicated in the occurrence and development of cardiovascular diseases. The differently expressed LncRNAs and their biological effects during RIPC have not been explored previously. In this study, mouse and human LncRNA microarrays were used to investigate the expression signatures of LncRNAs and mRNAs in the myocardial tissue after RIPC. Therafter, homology comparisons were used to screen homologous genes from differentially expressed LncRNAs. Competing endogenous RNA (ceRNA) mechanism analysis were employed to find the matching relationship among homologous LncRNA, mRNA and microRNA. 554 differentially expressed mouse LncRNAs (281 up-regulated/273 down-regulated) and 1392 differentially expresssed human LncRNAs (635 up-regulated/757 down-regulated) were selected for further analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to quantify these LncRNAs, homology comparison and ceRNA mechanism analysis provided a pair of homologous LncRNAs (ENST00000574727 & ENSMUST00000123752) for further research investigation. Overall, in this study, a number of differentially expressed LncRNAs were identified which may play an important role the regulation of both inflammation and cell proliferation. The findings may thus unveil the mystery of RIPC and discover a novel protective mechanism for the mitigation of cardiovascular ischemia-reperfusion disease.Skin flap ischemia-reperfusion (IR) injury is the key factor to the success rate of skin transplantation, the molecular mechanism of flap IR injury needs to be continuously explored to provide new ideas for its clinical treatment. G protein-coupled receptor kinase 2 (GRK2) was reported to be involved in regulating mitochondrial function, and mitochondria were essential in the process of flap IR. Thus, we aimed to investigate the function of GRK2 in flap ischemia-reperfusion injury and further explore the underlying mechanism. Sixty male C57BL/6 mice were randomly divided into four groups sham, IR+sh-NC, IR+sh-GRK2 and IR+sh-GRK2+ dynamin-related GTPase 1 (Drp1). Flap function and mitochondrial function were determined after ischemia for 3 hours and reperfusion for 72 hours. Comparing with sham group, GRK2 was increased in flap after IR injury. Loss of GRK2 inhibited cell apoptosis and promoted cell proliferation of flap after IR injury. And deficiency of GRK2 promoted mitochondrial function in flap after IR injury. IR injury up-regulated Drp1 expression in flap, while sh-GRK2 down-regulated Drp1 expression. Furthermore, overexpression of Drp1 removed the protective effect of sh-GRK2. selleck chemicals In conclusion, our study revealed that GRK2 deletion improved flap function and mitochondrial function by inhibiting Drp1 expression, which may provide a new insight for the clinical treatment of flap ischemia-reperfusion injury.This study aimed to investigate the protective effects of Schisandrin C during diabetic nephropathy (DN) treatment. After DN induction, mice were treated with Schisandrin C, and diabetic metabolic parameters and renal function-associated factors were measured. Renal structural damage was evaluated by hematoxylin and eosin (HE) and Masson's trichrome staining. Macrophage polarization and macrophage-mediated inflammatory factors were detected in the kidneys by immunohistochemistry (IHC) and enzyme-linked immunosorbent assay (ELISA), respectively. The Swiprosin-1/interferon (IFN)-γ-Rβ pathway was evaluated by western blot (WB) analysis. The preliminary effects of Schisandrin C in high-glucose-stimulated macrophages from DN mice were verified by flow cytometry, ELISA, and WB analyses. These results indicated that Schisandrin C significantly regulated physiological parameters in DN. Renal structural damage was mitigated by Schisandrin C. In Schisandrin-C-treated groups, the expression levels of CD86, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β decreased, whereas CD206, IL-10, and transforming growth factor (TGF)-β expression levels increased. In vitro experiments indicated that among CD86+ cells, TNF-α, IL-6, and IL-1β expression levels significantly decreased, whereas among CD206+ cells, IL-10 and TGF-β expression increased following Schisandrin-C-treatment. Finally, Schisandrin C inhibited the expression of Swiprosin-1, IFN-γ-Rβ, phospho-Janus kinase 2 (p-JAK2), phospho-signal transducer and activator of transcription 1 (p-STAT1), and p-STAT3, in both DN model mice and high-glucose-stimulated RAW264.7 cells. The present study indicated a novel use for Schisandrin C to suppress DN progression, by promoting M1 to M2 macrophage polarization. Schisandrin C exerted protective effects against DN by regulating the polarization-dependent Swiprosin-1/IFN-γ-Rβ signaling pathway in macrophages.

Recent evidence suggests prostate cancer independent of treatment has atrophic effects on whole heart and left ventricular (LV) masses, associated with reduced endurance exercise capacity. In a pre-clinical model, we tested the hypothesis that high-intensity training could prevent cardiac atrophy with prostate cancer and alter cardiac protein degradation mechanisms.

Dunning R-3327 AT-1 prostate cancer cells (1×10

) were injected into the ventral prostate lobe of 5-6 mo immunocompetent Copenhagen rats (n=24). These animals were randomized into two groups, tumor-bearing exercise (TBEX, n=15) or tumor bearing sedentary (TBS, n=9). Five days after surgery, TBEX animals began exercise on a treadmill (25 m/min, 15° incline) for 45-60 min/day for 18±2 days. Pre-surgery (Pre), and post-exercise training (Post) echocardiographic evaluation (Vivid S6, GE Health Care), using the parasternal short axis view, was used to examine ventricle dimensions. Markers of protein degradation (muscle atrophy F-box, Cathepsin B, Cathepsin L) in the left ventricle were semi-quantified via Western Blot.