Pentoxifylline ameliorates chronic stress/high-fat diet-induced vascular wall disease: the role of circulating endothelial progenitor cells

2019 ◽  
Vol 392 (6) ◽  
pp. 669-683 ◽  
Author(s):  
Jolly Mounir William Labib ◽  
Sawsan Aboul-Fotouh ◽  
Mohamed Z. Habib ◽  
Mohamed Abd Elrahman Ahmed Mekawy ◽  
Kawthar A. Farrag ◽  
...  
2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Chi-Hsuan Ko ◽  
Sung-Ling Yeh ◽  
Chiu-Li Yeh

This study investigated whether glutamine (GLN) pretreatment can enhance circulating endothelial progenitor cells (EPCs) and attenuate inflammatory reaction in high-fat diet-induced obese mice with limb ischemia. Mice were assigned to a normal control (NC), high-fat control (HC), limb ischemia (HI), and GLN limb ischemia (HG) groups. The NC group provided chow diet and treated as a negative control. Mice in the HC and HI groups were fed a high-fat diet which 60% energy provided by fat for 8 weeks. Mice in the HG group were fed the same diet for 4 weeks and then transferred to a high-fat diet with 25% of total protein nitrogen provided as GLN to replace part of the casein for the subsequent 4 weeks. After feeding 8 weeks, mice in the HC group were sham-operated, while the HI and HG groups underwent an operation to induce limb ischemia. All mice except the NC group were euthanized on either day 1 or 7 after the operation. The results showed that the 8 weeks’ high-fat diet feeding resulted in obesity. The HG group had higher circulating EPCs on day 1 while muscle vascular endothelial growth factor, matrix metalloproteinase-9, and hypoxia-inducible factor-1 gene expressions were higher on day 7 postischemia than those of the HI group. The superoxide dismutase activity and reduced glutathione content in affected muscles were higher, whereas mRNA expressions of interleukin-6 and tumor necrosis factor-α were lower in the HG than those in the HI group. These findings suggest that obese mice pretreated with GLN-supplemented high-fat diet increased circulating EPC percentage, enhanced the antioxidant capacity, and attenuated inflammatory reactions in response to limb ischemia.


2013 ◽  
Vol 61 (10) ◽  
pp. E1371
Author(s):  
Francesca Felice ◽  
Rossella Di Stefano ◽  
Stefano Pini ◽  
Gianfranco Mazzotta ◽  
Francesco M. Bovenzi ◽  
...  

2007 ◽  
Vol 98 (11) ◽  
pp. 930-939 ◽  
Author(s):  
Derya Tilki ◽  
Hans-Peter Hohn ◽  
Ursula Gehling ◽  
Nerbil Kilic ◽  
Süleyman Ergün

SummaryA rapidly increasing body of data suggests an essential role of endothelial progenitor cells (EPCs) in vascular regeneration, formation of new vessels in cardiovascular diseases and also in tumor vasculogenesis. Moreover, recent data obtained from clinical studies with anti-angiogenic drugs in tumor therapy or with pro-angiogenic stimuli in ischemic disorders implicate a predictive role of the number of EPCs circulating in the peripheral blood in monitoring of these diseases. However, there is still some controversial data regarding the relevance of the EPCs in vascular formation depending on models used and diseases studied. One of the essential prerequisites for a better understanding of the whole contribution of EPCs to vascular formation in adult, a process called postnatal vasculogenesis, is to identify their exact sources. We could recently discover the existence of EPCs in a distinct zone of the vascular wall of large and middle sized adult blood vessels and showed that these cells are capable to differentiate into mature endothelial cells, to form capillary sprouts in arterial ring assay and to build vasa vasorumlike structures within the vascular wall. They also can be mobilized very rapidly from the vascular wall by tumor cells. This review will discuss the functional implications of these vascular wall resident endothelial progenitor cells (VW-EPCs) in relation to those of EPCs circulating in peripheral blood or derived from the bone marrow in cardiovascular and neoplastic diseases.


Lung Cancer ◽  
2005 ◽  
Vol 49 ◽  
pp. S368-S369
Author(s):  
B. Dome ◽  
J. Timar ◽  
G. Ostoros ◽  
L. Meszaros ◽  
J. Dobos ◽  
...  

2015 ◽  
Vol 66 (6) ◽  
pp. 532-538 ◽  
Author(s):  
Martin Steinmetz ◽  
Eva Lucanus ◽  
Sebastian Zimmer ◽  
Georg Nickenig ◽  
Nikos Werner

2019 ◽  
Vol 32 (3) ◽  
pp. 770
Author(s):  
AsmaaS Abo El-Yazeed ◽  
LailaM Montaser ◽  
AhmedA Sonbol ◽  
AhmedS EL-Gammal

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y.-H Chan ◽  
M C Ngai ◽  
Y Chen ◽  
M Z Wu ◽  
Y J Yu ◽  
...  

Abstract Background Rheumatoid arthritis is associated with both abnormal bone metabolism and atherogenesis but mechanistic links were missing. Aim This study aimed to investigate the role of osteocalcin (OCN)-expressing circulating endothelial progenitor cells (EPC)s in the severity and dissemination of systemic arterial calcifications in rheumatoid arthritis. Methods We performed flow cytometry studies in 145 consecutive patients with rheumatoid arthritis to determine osteogenic circulating levels of OCN-positive (OCN+) CD34+KDR+ and OCN+CD34+, versus conventional early EPC CD34+CD133+KDR+. Total calcium load of the thoracic aorta (ascending plus descending) and the carotid arteries were assessed by non-contrast computed tomography (CT) and contrast CT angiography. Results Osteogenic EPCs OCN+CD34+KDR+ (P=0.002) and OCN+CD34+ were strikingly associated with the clustered presence of aortic and carotid calcification (P=0.002 and 0.001 respectively, Figure). Multivariable analyses revealed that circulating OCN+CD34+KDR+ (B=14.4 [95% CI 4.0 to 24.8], P=0.007) and OCN+CD34+ (B=9.6 [95% CI 4.9 to 14.3], P<0.001) remained independently associated with increased aortic calcium load. OCN+CD34+ EPC (B=0.8 [95% CI 0.1 to 1.5], P=0.023), but not OCN+CD34+KDR+ EPC (B=1.2 [95% CI −0.2 to 2.6], P=0.09) was further independently associated with carotid calcium load. In comparison, conventional early EPC CD34+CD133+KDR+ had no significant association with aortic or carotid calcium load (P=0.46 and 0.88, respectively). Conclusions Circulating level of osteogenic EPC is associated with promulgated aortic and carotid calcification in patients with rheumatoid arthritis, suggesting a potential mechanistic role of the bone-vascular axis in pro-atherogenicity of rheumatic diseases. Acknowledgement/Funding General Research Fund, Hong Kong Research Grants Council


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