Vitamin D [Biotin]

The skin has many functions, such as providing a barrier against injury and pathogens, protecting from ultraviolet light, and regulating body temperature. Mechanical causes and many different pathologies can lead to skin damage. Therefore, it is important for the skin to be always adaptable and renewable and for cells to undergo proliferation. Here, we demonstrate that 1 alpha, 25-dihydroxyvitamin D-3 (VD3) stimulates keratinocyte proliferation, leading to wound closure in a simulation model of injury. Functionally, our results show that VD3 acts by stimulating cyclin D1, a cyclin that promotes the G1/S transition of the cell cycle. The study on the mechanism underlying cyclin D1 expression upon VD3 stimulation clearly demonstrates a key role of neutral sphingomyelinase. The enzyme, whose gene and protein expression is stimulated by VD3, is itself able to induce effects on cyclin D1 and wound healing similar to those obtained with VD3. These results could be very useful in the future to better understand wound mechanisms and improve therapeutic interventions.

The pathogenesis of colon cancer (Cca) is to be further investigated. Vitamin D deficiency is associated with cancer growth; the underlying mechanism is unclear. Published data indicate that Cca cells express CD23. This study tests a hypothesis that exposure to IgE induces Cca cell apoptosis. In this study, the effect of ligation of CD23 by IgE on the expression of cyp27b1 was performed with Cca cells. The induction of apoptosis of Cca cells by IgE was assessed in a cell culture model. We observed that Cca cells express CD23; ligation of CD23 with IgE on Cca cells increased the expression of cyp27b1 in Cca, which promoted the conversion of VD3 to calcitriol, the latter increased the expression of FasL by Cca cells, and induced apoptosis of Cca cells. In conclusion, IgE is capable of inducing the cancer cell apoptosis via ligating CD23 and converting VD3 to calcitriol. The results suggest that IgE may have therapeutic potential in the treatment of Cca.