FGF23 also plays a central role in the pathogenesis of post-transplant hypophosphatemia in kidney transplant recipients. Furthermore, recent studies suggest that FGF23 could be an independent predictor of mortality in dialysis patients, indicating its potential role as a sensitive biomarker of disordered phosphate metabolism. This brief review summarizes recent insights into the role of FGF23 in the pathogenesis of mineral and bone disorders in CKD.”
“Objective: Effective induction of human mesenchymal stem cell (hMSC) differentiation
for regenerative medicine applications remains a great challenge. While much research has studied hMSC activity during differentiation, it is unclear whether KPT-330 concentration pre-differentiation culture can modulate differentiation capacity. We investigate the effect of glucose concentration in pre-differentiation/expansion culture on modulating chondrogenic capacity of hMSCs, and explore the underlying molecular mechanism.
Design: The extent of chondrogenesis of hMSCs previously cultured with different concentrations of glucose was evaluated. Transforming growth factor-beta (TGF-beta) signaling molecules and protein kinase C (PKC) were analyzed to identify selleckchem the role of these molecules in the regulation of glucose on chondrogenesis. In addition, hMSCs in high-glucose expansion culture were treated with the PKC inhibitor to modulate the activity
of PKC and TGF-beta signaling molecules.
Results: High-glucose maintained hMSCs were less chondrogenic than low-glucose maintained cells upon receiving differentiation signals. Interestingly, we found that high-glucose culture increased the phosphorylation of PKC and expression of type 3-Methyladenine chemical structure II TGF-beta receptor (TGF beta RII) in pre-differentiation hMSCs. However, low-glucose maintained hMSCs became more responsive to chondrogenic induction with increased PKC activation and TGF beta RII expression than high-glucose maintained hMSCs during differentiation. Inhibiting the PKC activity
of high-glucose maintained hMSCs during expansion culture upregulated the TGF beta RII expression of chondrogenic cell pellets, and enhanced chondrogenesis.
Conclusion: Our findings demonstrate the effect of glucose concentration on regulating the chondrogenic capability of pre-differentiation hMSCs, and provide insight into the mechanism of how glucose concentration regulates PKC and TGF-beta signaling molecules to prime pre-differentiation hMSCs for subsequent chondrogenesis. (C) 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.”
“The hallmark of IgA nephropathy (IgAN) is macroscopic hematuria coinciding with, or immediately following, a mucosal infection, usually of the upper respiratory airways. The role of mucosal pathogens has been proven in different experimental models.