In:
Journal of Vascular Research, S. Karger AG, Vol. 56, No. 1 ( 2019), p. 17-27
Abstract:
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-γ) 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-γ/HO-1 signaling pathway.
Type of Medium:
Online Resource
ISSN:
1018-1172
,
1423-0135
Language:
English
Publisher:
S. Karger AG
Publication Date:
2019
detail.hit.zdb_id:
1482726-8
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