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DOI 10.1016/j.biopha.2017.01.093

Медицинская библиотека · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2017

25-Hydroxyvitamin D-1-α-hydroxylase in apoliporotein E knockout mice: The role of protecting vascular smooth muscle cell from calcification.

Xiang Wei, Liao Wang, Yi Zhuwen, He Xiaojie, Ding Yan

СтатьяПеревод пока не подготовлен

Аннотация

Previous publications widely reported that 25-hydroxyvitamin D-1-α-hydroxylase (CYP27B1) regulated the metabolism of 25-hydroxyvitamin D3, which has a close association between altered activity of vitamin D and vascular calcification has been reported in various human diseases, including chronic kidney disease, osteoporosis and atherosclerosis. Vascular calcification is a clinically significant component of atherosclerosis and may be promoted by ROS associated inflammatory. In this study, we evaluated the effect of 25-hydroxyvitamin D-1-α-hydroxylase on the atherosclerosis disease both in apolipoprotein (apo) E-/- mice and wild-type mice. We also isolated endothelial cell (ECs) and vascular smooth muscle cells (VSMCs) in aortic from the wild type mice and apoE-/- mice respectively, then investigated that after parathyroid hormone (PTH) both of the CYP27B1 and vitamin D receptor (VDR) expressions in apoE-/-EC and apoE-/-VSMC were higher than the wide-type EC and VSMCs. However, the increased proliferation and decreased apoptosis have showed in EC and VSMC compared with the cells from apo E-/- mice. Moreover, the index associated with vascular calcification such as intracellular Ca2+ concentration and alkaline phosphatase (ALP) activity have been tested and the result suggested that the levels of the former index have improved in the apoE-/-EC and apoE-/-VSMC. We got similar conclusions under the pre-treatment with 1, 25(OH) 2D3.

Для цитирования: Xiang Wei, Liao Wang, Yi Zhuwen, He Xiaojie, Ding Yan. 25-Hydroxyvitamin D-1-α-hydroxylase in apoliporotein E knockout mice: The role of protecting vascular smooth muscle cell from calcification.. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2017. DOI: 10.1016/j.biopha.2017.01.093.

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