Vitamin D Receptor (Phospho-Ser208) ELISA Kit

The objective of this study was to investigate the dose-dependent effect of 1 alpha,25-(OH)(2)VD3 (Vit D-3) on in vitro proliferation of goat luteinised granulosa cells (LGCs) and to determine the underlying mechanisms of its action by overexpressing and silencing vitamin D receptor (VDR) in LGCs. Results showed that VDR was prominently localised in GCs and theca cells (TCs) and its expression increased with follicle diameter, but was lower in atretic follicles than in healthy follicles. The proliferation rate of LGCs was significantly higher in the Vit D-3-treated groups than in the control group, with the highest proliferation rate observed in the 10 nM group; this was accompanied by changes in the expression of cell cycle-related genes. These data indicate that Vit D-3 affects LGC proliferation in a dose-dependent manner. Contrary to the VDR knockdown effects, its overexpression upregulated and downregulated cell cycle- and apoptosis-related genes respectively; moreover, supplementation with 10 nM of Vit D-3 significantly enhanced these effects. These results suggest that changes in VDR expression patterns in LGCs may be associated with follicular development by regulation of cell proliferation and apoptosis. These findings will enhance the understanding of the roles of Vit D-3 and VDR in goat ovarian follicular development.

Background: This study aimed to investigate the mechanisms underlying the neuroprotective effects of vitamin D. Material/Methods: Rat primary neuron cells were incubated under a hypoxia condition [a hypoxic chamber mixed with anaerobic gas (90% N-2, 5% CO2) and 5% O-2] to induce cell injury. Cell transfection was performed to overexpress or suppress the expression of dual oxidase 1 (DUOX1). The malondialdehyde (MDA) and superoxide dismutase (SOD) levels were detected using a MDA (A003-2) or SOD (A001-1) kit. DUOX1 mRNA levels were detected using RT-PCR. Hypoxia-inducible factor-1 alpha (HIF-1 alpha), DUOX1, vitamin D receptor (VDR), NF-kappa B protein expressions were determined by western blotting. Cell apoptosis and reactive oxygen species (ROS) were evaluated by flow cytometry. Results: ROS increased significantly after hypoxic treatment. The expressions of HIF-1 alpha and DUOX1 were significantly increased after hypoxic treatment. Vitamin D could decrease ROS level, apoptotic neuron cells and DUOX1 expression, and increase VDR expression. Downregulation of DUOX1 significantly decreased MDA level and apoptotic percentages of neuron cells, increased SOD level, and counteracted the hypoxia-induced increase of NF-kappa B signal. Further study showed that overexpression of DUOX1 significantly increased MDA level, ROS level, apoptotic percentages of neuron cells, and NF-kappa B nuclear signaling, while decreased SOD level. Vitamin D significantly counteracted the effects of DUOX1 overexpression induced injury in rat primary neuron cells. Conclusions: Our study indicated that vitamin D may protect neuron cells from hypoxia-induced injury by regulating DUOX1 via the NF-kappa B signaling pathway.