1α, 25-Dihydroxyvitamin D3 up-regulates IL-34 expression in SH-SY5Y neural cells. Issue 7 (October 2017)

• Record Type: Journal Article
• Authors: Zhang, Dong; Li, Miaomiao; Dong, Yang; Zhang, Xinhui; Liu, Xingyun; Chen, Zhangming; Zhu, Yongji; Wang, Huiming; Liu, Xuwen; Zhu, Jialiang; Shen, Yujun; Korner, Heinrich; Ying, Songcheng; Fang, Shengyun; Shen, Yuxian
• Is Part Of: Innate immunity. Volume 23:Issue 7(2017:Oct.)
• Page Start: 584
• Page End: 591
• Publication Date: 2017-10
• Subjects: 1α -- 25-Dihydroxyvitamin D3 -- Alzheimer disease -- expression -- IL-34 -- neuronal cell; Natural immunity -- Periodicals; Endotoxins -- Periodicals; 616.07905
• DOI: 10.1177/1753425917725391
• Languages: English
• ISSNs: 1753-4259

Abstract

Vitamin D supplementation is regarded as a novel approach to treat Alzheimer's disease, but the underlying mechanism remains elusive. The cytokine IL-34 provides strong neuroprotective and survival signals in brain injury and neurodegeneration and could be an immunological mediator for the vitamin D-induced protection. The aim of this study was to investigate whether human IL-34 is up-regulated in neuronal cells by the hormonally active form of vitamin D, 1α, 25-dihydroxyvitamin D3 [1α, 25(OH)2 D3 ]. We found that IL-34 was detectable in a variety of cell lines and its expression was strongly induced in SH-SY5Y neural cells in a dose- and time-dependent manner by 1α, 25(OH)2 D3 through the vitamin D receptor (VDR). Furthermore, we identified the core promoter of IL-34 gene and a VDR binding site (CGCCCT) that was required for 1α, 25(OH)2 D3 -induced IL-34 expression. These findings suggest that the induction of IL-34 expression by 1α, 25(OH)2 D3 may constitute a mechanism that explains the protective function of vitamin D in Alzheimer's disease.