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This study clarified the role of Mir-217 in high glucose cultured rat glomerular mesangial cells through Sirt1/HIF-1α signaling pathway and provided new therapeutic targets for diabetic nephropathy. Copyright © 2016 John Wiley & Sons, Ltd.

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Our findings suggest that serum miR-130b may be a new biomarker for the early diagnosis of DN in T2DM. Circulating miR-130b may possibly be involved in the pathological mechanism of DN, such as lipid metabolic disorders, oxidative stress, extracellular matrix deposition and renal fibrosis.

Objective. To investigate the expression of miR-192 and its significance in diabetic nephropathy (DN) patients. Methods. 464 patients with type 2 diabetes mellitus (T2DM) were divided into normal albuminuria group (NA, n = 157), microalbuminuria group (MA, n = 159), and large amount of albuminuria group (LA, n = 148). 127 healthy persons were selected as the control group (NC, n = 127). The serum miR-192 levels were detected by Real-Time PCR and transforming growth factor-β1 (TGF-β1) and fibronectin (FN) were detected by enzyme-linked immunosorbent assay. The relationships among these parameters were analyzed by Pearson correlation analysis and multiple linear regression analysis. Results. The miR-192 in the LA group was significantly lower than other groups, which was lower in the MA group than in the NA group (P < 0.01). The TGF-β1 and FN in the LA group were significantly higher than other groups, which were higher in the MA group than in the NA group (P < 0.01). The expression of miR-192 was negatively correlated with TGF-β1, FN, and Ln (UACR) and miR-192, TGF-β1, and FN were independent relevant factors affecting Ln (UACR) in T2DM (P < 0.01). Conclusions. These findings indicate that the levels of miR-192 were lower accompanied by the decrease of urine albumin creatinine ratio (UACR) and the association between miR-192 and nephritic fibrosis in DN.

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Monitoring of cells in vivo after transplantation could supply important information for determining the efficacy of stem cell therapy. The use of quantum dots (QDs) has several advantages for in vivo imaging, such as remarkable resistance to photo bleaching, high fluorescence efficiency, and size-tunable emission. After they are taken up by cells via endocytosis, QDs lose their fluorescence intensity in endosomes/lysosomes at low pH because the intensity cannot survive under acidic conditions. Moreover, the amount of QD uptake by mesenchymal stem cells (MSCs) is extremely small. Therefore, for effective labeling of MSCs and long observation of MSCs labeled by QDs in vivo, it is essential both to increase cellular uptake of QDs and to promote endosomal escape into the cytosol. The polyamidoamine (PAMAM) dendrimer had plenty of cationic charge, which promoted cellular uptake though electrostatic interactions, and a "buffering capacity," which enhanced endosomal escape into the cytosol. In this study, QDs were modified with PAMAM dendrimer for the efficient labeling of MSCs by QDs. The uptake efficiency and cytosolic distribution of QDs in primary cultured MSCs were increased by the modification of the PAMAM dendrimer. The fluorescence intensity in MSCs labeled by PAMAM dendrimer-conjugated QDs lasted for a longer time in harvested culture plates or in cell-transplanted mice than that in MSCs labeled by non-conjugated QDs.

The aim of this study is to investigate the correlation between serum microRNA-217 and the severity of diabetic kidney disease determined by albuminuria. Four hundred ninety five type 2 diabetes patients were divided into three groups: normoalbuminuric group, microalbuminuric group, and macroalbuminuric group. Serum microRNA-217 levels were validated by real-time polymerase chain reaction. Serum silent information regulator 1, Hypoxia-inducible factor-1α and vascular endothelial growth factor were determined by enzyme-linked immunosorbent assay. Compared with control, serum microRNA-217 levels were significantly increased in type 2 diabetes patients and gradually increased in patients of normoalbuminuric, microalbuminuric, and macroalbuminuric groups (P < 0.01). Moreover, increased levels of serum microRNA-217, hypoxia-inducible factor-1α, vascular endothelial growth factor, diabetes mellitus duration, fasting blood glucose, fasting insulin, homeostasis model assessment for insulin resistance, glycated hemoglobin, low-density lipoprotein, total cholesterol, triglyceride, uric acid, serum creatinine, blood urea nitrogen, and decreased levels of serum silent information regulator 1 and high-density lipoprotein were significantly correlated with Ln(ACR) (P < 0.05). In addition, serum microRNA-217 was positively correlated with diabetes mellitus duration, homeostasis model assessment for insulin resistance, glycated hemoglobin, Ln(ACR), low-density lipoprotein, total cholesterol, triglyceride, uric acid, serum creatinine, blood urea nitrogen, hypoxia-inducible factor-1α, vascular endothelial growth factor (P < 0.05), and negatively correlated with serum silent information regulator 1 (P = 0.002). Our findings suggest that microRNA-217 may have an association with the development of proteinuria in type 2 diabetes patients. Serum microRNA-217 may be involved in the development of diabetic kidney disease by promoting chronic inflammation, renal fibrosis, and angiogenesis.