Journal
JOURNAL OF VASCULAR RESEARCH
Volume 56, Issue 1, Pages 17-27Publisher
KARGER
DOI: 10.1159/000496164
Keywords
Vitamin D; Angiotensin II; Endothelial progenitor cells; Vascular injury; Peroxisome proliferator-activated receptor-gamma; Heme oxygenase-1
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Funding
- National Key Research and Development Program [2016YFA0100800]
- National Natural Science Foundation of China [81671105]
- Fundamental Research Funds for the Central Universities
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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
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