Ryu ES, Kim MJ, Shin HS, Jang YH, Choi HS, Jo I, Johnson RJ, Kang DH. Uric acid-induced phenotypic transition of renal tubular cells as a novel mechanism of chronic kidney disease.

PURPOSEThis study aimed to identify the effects of the sintering conditions of dental zirconia on the grain size and translucency.MATERIALS AND METHODSTen specimens of each of two commercial brands of zirconia (Lava and KaVo) were made and sintered under five different conditions. Microwave sintering (MS) and conventional sintering (CS) methods were used to fabricate zirconia specimens. The dwelling time was 20 minutes for MS and 20 minutes, 2, 10, and 40 hours for CS. The density and the grain size of the sintered zirconia blocks were measured. Total transmission measurements were taken using a spectrophotometer. Two-way analysis of variance model was used for the analysis and performed at a type-one error rate of 0.05.RESULTSThere was no significant difference in density between brands and sintering conditions. The mean grain size increased according to sintering conditions as follows: MS-20 min, CS-20 min, CS-2 hr, CS-10 hr, and CS-40 hr for both brands. The mean grain size ranged from 347-1,512 nm for Lava and 373-1,481 nm for KaVo. The mean light transmittance values of Lava and KaVo were 28.39-34.48% and 28.09-30.50%, respectively.CONCLUSIONDifferent sintering conditions resulted in differences in grain size and light transmittance. To obtain more translucent dental zirconia restorations, shorter sintering times should be considered.

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The insulin-like growth factor (IGF) signaling pathway plays a crucial role in the regulation of cell growth, differentiation, apoptosis, and aging. IGF-binding proteins (IGFBPs) are important members of the IGF axis. IGFBP-5 is up-regulated during cellular senescence in human dermal fibroblasts and endothelial cells, but the function of IGFBP-5 in cellular senescence is unknown. Here we show that IGFBP-5 plays important roles in the regulation of cellular senescence. Knockdown of IGFBP-5 in old human umbilical endothelial cells (HUVECs) with IGFBP-5 micro-RNA lentivirus caused partial reduction of a variety of senescent phenotypes, such as changes in cell morphology, increases in cell proliferation, and decreases in senescence-associated beta-galactosidase (SA-beta-gal) staining. In addition, treatment with IGFBP-5 protein or up-regulation of IGFBP-5 in young cells accelerates cellular senescence, as confirmed by cell proliferation and SA-beta-gal staining. Premature senescence induced by IGFBP-5 up-regulation in young cells was rescued by knockdown of p53, but not by knockdown of p16. Furthermore, atherosclerotic arteries exhibited strong IGFBP-5-positive staining along intimal plaques. These results suggest that IGFBP-5 plays a role in the regulation of cellular senescence via a p53-dependent pathway and in aging-associated vascular diseases.

Myoblast fusion is essential for the formation of skeletal muscle myofibres. Studies have shown that phosphatidylserine is necessary for myoblast fusion, but the underlying mechanism is not known. Here we show that the phosphatidylserine receptor stabilin-2 acts as a membrane protein for myoblast fusion during myogenic differentiation and muscle regeneration. Stabilin-2 expression is induced during myogenic differentiation, and is regulated by calcineurin/NFAT signalling in myoblasts. Forced expression of stabilin-2 in myoblasts is associated with increased myotube formation, whereas deficiency of stabilin-2 results in the formation of small, thin myotubes. Stab2-deficient mice have myofibres with small cross-sectional area and few myonuclei and impaired muscle regeneration after injury. Importantly, myoblasts lacking stabilin-2 have reduced phosphatidylserine-dependent fusion. Collectively, our results show that stabilin-2 contributes to phosphatidylserine-dependent myoblast fusion and provide new insights into the molecular mechanism by which phosphatidylserine mediates myoblast fusion during muscle growth and regeneration.