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[Display omitted] • The 3D hierarchical MIL-53(Fe) was directly in-situ grown on the Fe Foam through the semi-sacrificial template strategy. • The optimized self-supporting electrode can run at 100 mA cm−2 for 520 h without visible decrease in activity. • MIL-53(Fe) structures was completely in-situ self-reconstructed into metal oxyhydroxides with O v after the running OER for 2 h. • DFT calculations reveal that the FeOOH with rich O v transformed from MIL-53(Fe) facilitate the OER catalytic activity. • This work provides a quick and easy method to construct a advanced self-supporting electrodes based on MOFs. The exploitation of efficient, stable and cheap electrocatalyst for oxygen evolution reaction (OER) is very significant to the development of energy technology. In this study, Fe-based metal–organic frameworks (MIL-53(Fe)) self-supporting electrode with a 3D hierarchical open structure was developed through a semi-sacrificial strategy. The self-supporting electrode exhibits an excellent OER performance with an overpotential of 328 mV at 100 mA cm−2 in 1 M KOH, which is superior than that of IrO 2 catalyst. Importantly, the optimized self-supporting electrode could operate at 100 mA cm−2 for 520 h without visible decrease in activity. It was also found that the structure of MIL-53(Fe) was in-situ self-reconstructed into oxyhydroxides during OER process. However, the 3D hierarchical open structure assembled with nano-microstructures kept well, which ensured the long-term stability of our self-supporting electrode for OER. Furthermore, density functional theory (DFT) calculations reveal that the FeOOH with rich oxygen vacancy transformed from MIL-53(Fe) plays a key role for the OER catalytic activity. And, the uninterrupted formation of oxygen vacancy during OER process ensures the continuous OER catalytic activity, which is the original source for the ultra-long stability of the self-supporting electrode toward OER. This work explores the way for the construction of efficient self-supporting oxygen electrodes based on MOFs. [ABSTRACT FROM AUTHOR]

Diabetic nephropathy (DN) is among the common complications of diabetes and is a major cause of end-stage kidney disease. Emerging data indicate that renal inflammation is involved in DN progression and aggravation. Still, the exact cellular mechanisms remain unclear. Dysregulated expression of microRNAs (miRNAs) is associated with multiple diseases, including DN. The relationship between miRNAs and inflammation in DN is also unexplored. Here, we evaluated the role of miR-485 in mediating the response of human mesangial cells (HMCs) to a high glucose (HG) concentration, and the potential underlying mechanism. We found that miR-485 expression is significantly decreased in HG-stimulated HMCs. Overexpression of miR-485 suppressed HG-induced proliferation of HMCs. Lower production of proinflammatory cytokines (i.e., TNF-α, IL-1β, and IL-6) was observed in miR-485–overexpressing HMCs. Overexpression of miR-485 markedly suppressed the overexpression of extracellular-matrix proteins, e.g., collagen IV (Col IV) and fibronectin (FN), in HG-stimulated HMCs. Furthermore, miR-485 suppressed the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 5 (NOX5), restrained the HG-induced HMC proliferation, downregulated the expression of proinflammatory cytokines, and inhibited the production of extracellular-matrix proteins in HMCs. These results provide new insights into the involvement of the miR-485–NOX5 signaling pathway in DN progression. • miR-485 is significantly downregulated in HG-stimulated HMCs. • miR-485 inhibits HG-induced proliferation of HMCs. • miR-485 suppresses HG-induced oxidative stress, ECM production, and inflammation signs in HMCs. • NOX5 attenuates the inhibitory actions of miR-485 in HG-stimulated HMCs. [ABSTRACT FROM AUTHOR]

Emerging evidence has shown that microRNAs (miRNAs) play a mediatory role in the pathogenesis of diabetic nephropathy (DN), but the function of the involved miRNAs is still incomplete. Here, we found that miR-455-3p was down-regulated in the human mesangial cells (HMC) and human proximal tubule epithelial cells (HK-2) stimulated with high glucose (HG) or transforming growth factor beta 1 (TGF- β 1). Rho-associated coiled coil-containing protein kinase 2 ( ROCK2 ) was identified as a directed target of miR-455-3p. Overexpression of ROCK2 significantly attenuated the inhibitory effects of miR-455-3p on cell proliferation, extracellular matrix (ECM) synthesis and epithelial-mesenchymal transition (EMT) in HG-treated cells. Furthermore, the DN model was prepared by using high-fat feeding combined with Streptozotocin (STZ) induced rats, and the DN group was treated by injecting miR-455-3p agomir. The results of periodic acid-Schiff (PAS) and Masson staining showed that miR-455-3p overexpression improved the pathological changes of glomerular hypertrophy, mesangial amplification, and renal fibrosis. Additionally, miR-455-3p overexpression decreased ROCK2, proliferating cell nuclear antigen (PCNA) and Collagen I levels, and also reduced inflammatory cytokines TNF- α , MCP-1 and IL-1 β levels in vivo . Altogether, these results suggest that miR-455-3p plays an essential role in the treatment of renal fibrosis through repressing ROCK2 expression; and miR-455-3p might be an effective therapy for DN. [ABSTRACT FROM AUTHOR]