Profile analysis reveals transfer RNA fragments involved in mesangial cells proliferation.

Mesangial cell (MCs) proliferation is an essential component of glomerulonephritis. To find some bio-markers of mesangial cell proliferation, we investigate the relationship between transfer RNA fragments (tRFs) and proliferating mesangial cells. The model of proliferating mesangial cells was built by using transforming growth factor-1(TGF-ß1) treated mesangial cells. Then we analyzed the expression of tRFs in normal mesangial cells and mesangial cells treated by TGF-ß1 through high-throughput sequencing technique. qRT-PCR was conducted to validate the differently expressed tRFs in normal mesangial cells and mesangial cells treated by TGF-ß1. tDR-000064 and tDR-000103 were notably down-regulated in mesangial cells treated by TGF-ß1 compared with normal mesangial cells. Then we confirmed that tDR-000064 and tDR-000103 were correlated with proliferation of mesangial cells through receiver operating characteristic curve analysis. Furthermore, Gene ontology (GO) and pathway analysis demonstrated that the two dys-regulated tRFs were mostly involved in mesangial cells and TGF-ß1 receptor-mediated signaling pathway. Our research provides a comprehensive analysis of tRFs in proliferating mesangial cells. (Figure 1A).

Carboxylcellulose hydrogel confined-Fe3O4 nanoparticles catalyst for Fenton-like degradation of Rhodamine B.

Facile preparation of functional hydrogel materials for environmental catalysis is a hot research topic of soft materials science and green catalysis. In this study, a carboxylcellulose hydrogel confined Fe3O4 nanoparticles composite catalyst (Fe3O4@CHC) with magnetic recyclability has been synthesized by taking the advantages of the newly developed cellulose solution in tetramethyl guanidine/DMSO/CO2 through in situ acylation using mixed cyclic anhydrides and ion exchange reaction. The achieved Fe3O4@CHC hydrogel catalyst was shown to be an more efficient and better Fenton-like catalyst for decomposition of the organic dye rhodamine B (RhB) in the presence of hydrogen peroxide, with almost complete decomposition occurring within 180 min, in comparison with Fe3O4@cellulose hydrogel (CH) with excellent recyclability. This work provided a facile strategy for the preparation of hydrogel-based functional composite green catalytic materials, which has potential applications in green catalysis.

Connexin 43­autophagy loop in the podocyte injury of diabetic nephropathy.

The reduction of podocyte injury is a key strategy in controlling proteinuria, which is the main early clinical manifestation of diabetic nephropathy (DN). Impaired autophagic flux is the primary mechanism responsible for podocyte injury in DN. The aim of the present study was to elucidate the effect of connexin 43 (Cx43) on impaired autophagic flux in podocyte injury and to explore its molecular mechanism of action in DN. Sprague­Dawley rats were administered streptozocin (STZ) to construct a DN animal model. Podocytes were incubated in media containing either buffer or high glucose (HG; 30 mM) for variable time periods. The podocytes were then examined and the mechanism of injury was investigated using an Annexin V/PI assay, immunofluorescence staining, western blotting, and RNA interference. In vivo, STZ­induced DN rats with or without Cx43 knockdown were established to observe the role of Cx43 in autophagic flux and podocyte injury. We observed that HG induced podocyte injury, accompanied by increases in Cx43 expression and impaired autophagic flux, as evidenced by the accumulation of LC3II/LC3I and p62. Interestingly, the silencing of Cx43 expression ameliorated autophagic flux impairment and reduced podocyte injury via suppression of the mammalian target of rapamycin pathway. Furthermore, impaired autophagic flux also blocked the degradation of Cx43. In vitro studies indicated that higher numbers of Annexin V/PI­positive podocytes, impaired autophagic flux and increased Cx43 expression were observed in HG­induced podocyte injury relative to the control group. The pathogenic effect of Cx43 on impaired autophagic flux and podocyte injury was also confirmed by Cx43 knockdown. The present study provided preliminary evidence indicating that the interdependence of Cx43 and impaired autophagic flux represents a novel mechanism of podocyte injury in DN. Hence, the Cx43­autophagy loop is a potentially relevant therapeutic target for the treatment of DN.

Gene expression profiling analysis reveals that the long non­coding RNA uc.412 is involved in mesangial cell proliferation.

Hyperproliferation of mesangial cells (MCs) is the central pathological feature observed in certain human renal diseases. Furthermore, the long non­coding RNA uc.412 is regulated by transforming growth factor ß1 in mesangial cells in vitro. The present study aimed to investigate whether uc.412 serves a role in renal fibrosis and whether it may be considered as a therapeutic target in mesangial proliferative kidney diseases. The results demonstrated that uc.412 overexpression significantly increased MC proliferation. The transcriptional profile of MCs overexpressing uc.412 was assessed by RNA sequencing. A total of 462 up­ and 843 downregulated genes were identified (|fold change| ≥1.5), and reverse transcription­quantitative PCR was used to determine the expression of these differentially expressed genes (DEGs). Subsequently, the potential function of these DEGs was determined by bioinformatics analyses. The results indicated that these DEGs were involved in numerous signaling pathways associated with MC proliferation. The downstream association between up­ and downregulated genes was constructed via the STRING database. The protein­protein interaction network indicated that serpin family E member 1 and matrix metallopeptidase 3 may be hub proteins. In conclusion, the present study provided novel insight into the role of uc.412 in MC proliferation, which may aid in the development of novel treatment for mesangial proliferative kidney diseases.