Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway
Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway
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维生素 D 通过 PPAR-gamma/HO-1 途径改善血管紧张素 II 诱导的人内皮祖细胞损伤
DOI：
10.1159/000496164
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发表时间：
2019-01-01
影响因子：
1.7
通讯作者：
Zhu, Rongrong
中科院分区：
文献类型：
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作者：
Xu, Wei;Hu, Xiao;Zhu, Rongrong
维生素D对慢性炎症性疾病有重要的保护作用。血管紧张素II(AngII)触发血管损伤，并通过包括炎症在内的几种机制在血管疾病中发挥关键作用。相反，维生素D已被证明对慢性炎症有重要的保护作用。有证据表明，维生素D可以逆转血管紧张素转换酶的作用，但其发生的分子机制尚不清楚。我们的结果表明，维生素D可提高经血管紧张素转换酶抑制剂处理的内皮祖细胞的活力、迁移能力和管状形成，并抑制血管紧张素转换酶诱导的内皮前体细胞的凋亡。维生素D还逆转了血管紧张素转换酶诱导的内皮细胞的活性氧产生、血管炎症细胞因子的产生和核因子-kappa-B的激活。此外，用PPAR-γ的拮抗剂GW9662或siHO-1预处理EPC可减弱维生素D对血管紧张素Ⅱ诱导的EPC损伤的保护作用。总体而言，我们的数据表明，维生素D通过降低氧化应激和炎性细胞因子水平来改善血管紧张素转换酶诱导的异常EPC损伤。这些发现还表明，维生素D通过激活PPAR-γ/HO-1信号通路来保护血管内皮细胞免受血管紧张素Ⅱ诱导的血管损伤。(C)2019年S.Karger AG，巴塞尔
Vitamin D has an important protective effect on chronic inflammatory disease. Angiotensin II (AngII) triggers vascular damage and plays a key role in vascular diseases via several mechanisms, including inflammation. Conversely, vitamin D has been shown to have an important protective effect on chronic inflammation. There is evidence showing that vitamin D can reverse the effects of AngII, but the molecular mechanisms by which this occurs are not known. Our results demonstrate that vitamin D improved the viability, migration ability, and tube formation of AngII-pretreated endothelial progenitor cells (EPCs) and inhibited the apoptosis of EPCs induced by AngII. Vitamin D also reversed reactive oxygen species production, vascular inflammatory cytokine generation, and nuclear factor kappa-B activation in EPCs induced by AngII. Furthermore, EPC pretreatment with GW9662 (the antagonist for PPAR-gamma) or siHO-1 decreased the protective effect of vitamin D on AngII-induced EPC injury. Overall, our data indicate that vitamin D ameliorated AngII-induced abnormal EPC injury by decreasing oxidative stress and inflammatory cytokine levels. These findings also suggest that vitamin D protected EPCs from AngII-induced vascular injury via the activation of the PPAR-gamma/HO-1 signaling pathway. (C) 2019 S. Karger AG, Basel