Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

2019 ◽  
Vol 56 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Wei Xu ◽  
Xiao Hu ◽  
Xi Qi ◽  
Rui Zhu ◽  
Chen Li ◽  
...  
2012 ◽  
Vol 2 (3) ◽  
pp. 211 ◽  
Author(s):  
M. Grundmann ◽  
M. Haidar ◽  
S. Haß ◽  
C.A. Hubel ◽  
F. von Versen-Höynck

2008 ◽  
Vol 31 (4) ◽  
pp. 757-765 ◽  
Author(s):  
Toshio Imanishi ◽  
Katsunobu Kobayashi ◽  
Akio Kuroi ◽  
Hideyuki Ikejima ◽  
Takashi Akasaka

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0158672 ◽  
Author(s):  
Yu Dong ◽  
Qi Sun ◽  
Teng Liu ◽  
Huanyuan Wang ◽  
Kun Jiao ◽  
...  

2008 ◽  
Vol 294 (2) ◽  
pp. F379-F384 ◽  
Author(s):  
Peter E. Westerweel ◽  
Krista den Ouden ◽  
Tri Q. Nguyen ◽  
Roel Goldschmeding ◽  
Jaap A. Joles ◽  
...  

Impaired glomerular endothelial integrity is pivotal in various renal diseases and depends on both the degree of glomerular endothelial injury and the effectiveness of glomerular endothelial repair. Glomerular endothelial repair is, in part, mediated by bone marrow-derived endothelial progenitor cells. Peroxisome proliferator activated receptor-γ (PPAR-γ) agonists have therapeutic actions independent of their insulin-sensitizing effects, including enhancement of endothelial progenitor cell function and differentiation. We evaluated the effect of PPAR-γ agonist rosiglitazone (4 mg·kg−1·day−1) on the course of anti-Thy1-glomerulonephritis in rats. Rosiglitazone limited the development of proteinuria and prevented plasma urea elevation (8.1 ± 0.4 vs. 12.5 ± 1.1 mmol/l, P = 0.002). Histologically, inflammatory cell influx was not affected, but rosiglitazone-treated rats did show fewer microaneurysmatic glomeruli on day 7 (26 ± 3 vs. 41 ± 5%, P = 0.01) and reduced activation of matrix production with reduced renal cortical transforming growth factor-β, plasminogen activator inhibitor type 1, and fibronectin-1 mRNA expression. However, bone marrow-derived endothelial cell glomerular incorporation was not enhanced (3.1 ± 0.4 vs. 3.6 ± 0.3 cells/glomerular cross section; P = 0.31). Rosiglitazone treatment in nonnephritic rats did not influence proteinuria, urea, or renal histology. In conclusion, treatment with PPAR-γ agonist rosiglitazone ameliorates the course of experimental glomerulonephritis in a nondiabetic model, but not through enhancing incorporation of bone marrow-derived endothelial cells in the glomerulus.


PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e98527 ◽  
Author(s):  
Lars Brodowski ◽  
Jennifer Burlakov ◽  
Ashley C. Myerski ◽  
Constantin S. von Kaisenberg ◽  
Magdalena Grundmann ◽  
...  

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