骨化三醇受体
银屑病
发病机制
维生素D与神经学
医学
炎症
RAR相关孤儿受体γ
受体
维甲酸
孤儿受体
内分泌学
内科学
免疫学
作者
Anna A. Brożyna,Michał A. Żmijewski,Kinga Linowiecka,Tae‐Kang Kim,Radomir M. Slominski,Andrzej T. Slominski
摘要
The pathogenesis of inflammatory skin diseases is associated with the abnormal activity of keratinocytes and immune cells infiltrate. Vitamin D3 deficiency can correlate with the increased incidence, severity and duration of inflammatory skin disorders. The exact mechanism on how vitamin D3 influences inflammatory skin diseases still requires clarification. However, it can be associated with the disturbances in transmembrane glycoprotein-LRP2/megalin, which is implicated in vitamin D3 transport to the cell, and defects in vitamin D-signalling through the nuclear receptors. Therefore, by using immunohistochemistry, we analysed the expression of LRP2/megalin, VDR, RORα and RORγ in allergic contact dermatitis, lichen simplex chronicus, sarcoidosis and psoriasis in comparison with the normal skin. We observed decreased expression of LRP2/megalin in all inflammatory lesions in comparison with the normal skin. Significant differences were also noticed in VDR, RORα and RORγ levels between inflammatory lesions and normal skin. Our research indicates disturbed expression of LRP2/megalin, VDR, RORα and RORγ in inflammatory skin lesions in comparison with normal skin. Therefore, we suggest that changes in the activity of these proteins may play role in pathogenesis of inflammatory skin disorders. Furthermore, we suggest that LRP2/megalin, VDR, RORα and RORy may serve as targets in therapy of these diseases.
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