Lncrna CASC11 aggravates diabetic nephropathy via targeting FoxO1.

Background: To explore the biological effects of CASC11 on aggravating diabetic nephropathy (DN) by regulating FoxO1 (forkhead transcription factor O1). Methods: Serum levels of CASC11 and FoxO1 in DN patients were detected. The possibility of CASC11 in predicting the onset of DN was analyzed by depicting ROC curves. Correlation between CASC11 and FoxO1 was evaluated by Pearson correlation test. After intervening CASC11 and FoxO1 levels, we found that changes in proliferative and migratory abilities in high glucose (HG)induced kidney mesangial cells were determined respectively. Protein levels of TGF-ß1 and Smads regulated by both CASC11 and FoxO1 were examined by Western blot.

Circular RNA expression alterations and function prediction in OSA-induced pancreatic injury in mice: New insights into pathogenesis.

OBJECTIVES: Increasing studies have shown that circular RNAs (circRNAs) participate in the pathogenesis and progression of many diseases. However, the function of circRNAs in obstructive sleep apnea (OSA)-induced pancreatic damage has not been fully elucidated. In this study, the altered circRNA profiles in a chronic intermittent hypoxia (CIH) mouse model were investigated, aiming to provide novel clues for delineating the underlying mechanisms of OSA-induced pancreatic injury. METHODS: A CIH mouse model was established. circRNA microarray was then applied to profile circRNA expression in pancreatic samples from CIH groups and controls. Our preliminary findings were validated by qRT-PCR. Subsequently, GO and KEGG pathway analyses were carried out to annotate the biological functions of target genes of circRNAs. Lastly, we constructed a circRNA-miRNA-mRNA (ceRNA) network according to the predicted circRNA-miRNA and miRNA-mRNA pairs. RESULTS: A total of 26 circRNAs were identified to be differentially expressed, with 5 downregulated and 21 upregulated in the CIH model mice. Six selected circRNAs were preliminarily used to confirm the results by qRT-PCR, which were consistent with microarray. GO and pathway analysis indicated that numerous mRNAs were involved in the MAPK signaling pathway. The ceRNA analysis displayed the broad potentials of the dysregulated circRNAs to modulate their target genes by acting as miRNAs sponges. CONCLUSIONS: Taken together, our study first revealed the specific expression profile of circRNAs in CIH-induced pancreatic injury, which suggested a novel focus for investigating the molecular mechanism of OSA-induced pancreatic damage through modulating circRNAs.

Rehabilitation effects of circuit resistance training in coronary heart disease patients: A systematic review and meta-analysis.

BACKGROUND AND HYPOTHESIS: The rehabilitation effect of circuit resistance training in coronary heart disease (CHD) patients remains unclear. We perform this review to examine the rehabilitation effect of circuit resistance training in CHD patients and to provide a basis for the formulation of reasonable individual exercise prescriptions for CHD patients. METHODS: Randomized controlled trials (RCTs) were searched on PubMed, Web of Science, The Cochrane Library, Embase, Clinical Trials, and CNKI. About 1232 studies were identified. Nine RCTs were finally used for the present meta-analysis to determine the rehabilitation effect of circuit resistance training in CHD patients, compared to aerobic training. Individuals enrolled for the studies were at a mean age of 60.5 years old and were all CHD patients. Following the PRISMA guidelines, we extracted basic information about the study and patient characteristics, as well as measurements (e.g., the peak oxygen uptake, the body mass index [BMI], the body fat percentage, the systolic blood pressure, the total cholesterol, and triglycerides). Subsequently, this meta-analysis determined the overall effect by using standardized mean difference (SMD) and 95% confidence interval (CI). RESULTS: Compared with aerobic training, circuit resistance training significantly decrease the BMI and the body fat percentage. CONCLUSIONS: As suggested from the present meta-analysis of RCTs, circuit resistance training is effective in improving the BMI and the body fat percentage in CHD patients and may help delay the progression of CHD. CRT has the advantage of lower load in most cases with a similar effect.

miR­212 promotes renal interstitial fibrosis by inhibiting hypoxia­inducible factor 1­α inhibitor.

Renal interstitial fibrosis is one of the common causes, and a major pathological basis for the development of various types of chronic progressive renal to end­stage renal diseases. Therefore, it is important to clarify the underlying mechanisms of disease progression in order to develop effective strategies for the treatment and prevention of these pathologies. The aim of the present study was to investigate the association between microRNA (miR)­212 expression and the development of renal interstitial fibrosis, as well as analyzing the role of miR­212 in the disease. The expression of miR­212 was significantly increased in the peripheral blood of patients with renal interstitial fibrosis and in the kidney tissues of unilateral ureteral obstruction (UUO) mice. Angiotensin (Ang) II, TGF­ß1 and hypoxia were found to increase the expression of miR­212 and α smooth muscle actin (α­SMA) in NRK49F cells. Ang II stimulation induced the expression of miR­212 and α­SMA in NRK49F cells, while transfection of miR­212 mimics further upregulated the expression of α­SMA. miR­212 was also revealed to target hypoxia­inducible factor 1α inhibitor (HIF1AN) and to upregulate the expression of hypoxia­inducible factor 1α, α­SMA, connective tissue growth factor, collagen α­1(I) chain and collagen α­1(III) chain, whereas HIF1AN overexpression reversed the regulatory effects of miR­212. In UUO mice, miR­212 overexpression promoted the progression of renal interstitial fibrosis, whereas inhibiting miR­212 resulted in the opposite effect. These results indicated that high expression of miR­212 was closely associated with the occurrence of renal interstitial fibrosis, and that miR­212 may promote its development by targeting HIF1AN.

miR-19 promotes development of renal fibrosis by targeting PTEN-mediated epithelial-mesenchymal transition.

In recent years, it has been found that miRNA may play an important role in the field of gene regulation; miRNAs can participate in the regulation of various physiologic processes such as cell differentiation, proliferation, apoptosis, metabolism, and insulin secretion by regulation of target genes. The purpose of this study is to observe the relationship between the expression of miR-19 and renal fibrosis, to analyze the regulatory effect of miR-19 on renal tubular EMT, and to reveal its role and working mechanism in renal fibrosis. We found that the expression of miR-19 was significantly increased in peripheral blood of patients with renal fibrosis, in renal tissue of unilateral ureteral occlusion (UUO) mice, and in NRK-52E cells treated with TGF-ß1. Overexpression of miR-19 could decrease the expression of E-cadherin and increase the expression of α-SMA and fibronectin, while inhibition of miR-19 reverses TGF-ß1-induced EMT. Further studies revealed that miR-19 could inhibit its expression by binding to the 3'-UTR of PTEN. MiR-19 inhibitor or Akt inhibitor blocks phospho-Akt by TGF-ß1, and Akt inhibitors block miR-19 mimic-induced EMT. In UUO mice, overexpression of miR-19 promoted the development of renal fibrosis, while inhibition of miR-19 expression produced the opposite result. These results indicate that abnormal expression of miR-19 is associated with renal fibrosis. Moreover, miR-19 activates the Akt signaling pathway by targeting PTEN, and induces EMT in renal tubular epithelial cells, thereby promoting renal fibrosis.