The aim of this study was to explore whether progranulin (PGRN) can be a useful marker not only for accurate diagnosis of patients with active lupus nephritis (LN), but also for prediction of the disease activity in this population. A total of 154 LN patients were enrolled in this study, 76 of which were diagnosed as having active LN and 78 as having stable LN. Additionally, 71 age-matched non-LN patients were enrolled as controls. The serum and urine PGRN levels of each study population were measured using the enzyme-linked immunosorbent assay method. The diagnostic performance of both indicators and their correlation with the disease activity of LN were systematically investigated using receiver operating characteristic (ROC) analysis and correlation analysis. The active LN population had significantly higher serum and urine PGRN levels than the other two populations. ROC analysis further demonstrated that these two indicators, particularly in combination, appear to have a strong performance in discriminating active LN patients from the rest of the LN population. In the active LN population, serum and urine PGRN levels were not only significantly correlated with SLEDAI score, rSLEDAI score, and activity index, but also had a considerable association with several key markers reflecting the disease activity of LN, including serum levels of complement component 3 and ds-DNA. Nevertheless, neither of the two indicators were correlated with the pathological classification of LN, chronicity index, serum creatinine level, and 24-h urine protein levels. Our findings demonstrate that PGRN may have great potential as a diagnostic factor for active LN and as a predictor for its disease activity.
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, changes in proliferative and migratory abilities in HG-induced kidney mesangial cells were determinedrespectively. Expression levels of TGF-β1 and Smads regulated by both CASC11 and FoxO1 were examined by Western blot. Results: CASC11 was highly expressed in serum of DN patients, whereas FoxO1 was downregulated, showing a negative correlation. CASC11 may be a diagnostic marker for DN. It attenuated proliferative and migratory abilities in HG-induced kidney mesangial cells, and the inhibitory effects of CASC11 could be abolished by overexpression of FoxO1. Protein levels of TGF-β1 and Smads were positively regulated by CASC11, which were reversed by Smads regulation. Conclusions: Through activating the TGF-β1/Smads signaling, CASC11 inhibits FoxO1 expression and thus induces the aggravation of DN.
The present study investigates the potential role of dioscin (DIO) in the lipopolysaccharide (LPS)-induced kidney injury. For this purpose, DIO-loaded zein nanoparticles (DIO-ZNPs) were formulated and evaluated for physicochemical parameters. The DIO-ZNPs exhibited a controlled release of drug compared with that of the free drug suspension. Results showed that the cell viability of NRK-52E consistently decreased with the increase in LPS from 0.01 µg/ml to 2 µg/ml. When compared with LPS, DIO-induced NPs showed 1.10-, 1.32-, 1.57-and 1.92-fold increase in the cell viability for concentrations of 20 µg/ml, 50 µg/ml, 100 µg/ml and 200 µg/ml, respectively. DIO-ZNPs exhibited the most remarkable recovery in the cell proliferation compared with free DIO as shown by the cellular morphology analysis. Furthermore, Annexin-V staining analysis showed that the LPS-treated cells possess the lowest green fluorescence indicating fewer viable cells, whereas DIO-ZNPs exhibited the maximum green fluorescence comparable with that of the non-treated cells indicating maximum cell viability. Furthermore, the results show that DIO-ZNPs significantly increased the expression of miR-let-7i in the epithelial kidney cells, whereas the expression levels of TLR4 were significantly downregulated compared with that of the LPS-treated cells. In conclusion, miR-let-7i could be an interesting therapeutic target and nanoparticle-based DIO could be a potential candidate in the management of acute kidney injuryThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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