scholarly journals Hyperglycemia Accelerated Endothelial Progenitor Cell Senescence via the Activation of p38 Mitogen-Activated Protein Kinase

2006 ◽  
Vol 70 (8) ◽  
pp. 1076-1081 ◽  
Author(s):  
Shintaro Kuki ◽  
Toshio Imanishi ◽  
Katsunobu Kobayashi ◽  
Yoshiki Matsuo ◽  
Masahiro Obana ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Cell Senescence ◽  
Mitogen Activated Protein Kinase ◽  
Endothelial Progenitor ◽  
Mitogen Activated Protein

scholarly journals Deferoxamine accelerates endothelial progenitor cell senescence and compromises angiogenesis

Aging ◽  
2021 ◽  
Vol 13 (17) ◽  
pp. 21364-21384
Author(s):  
Yi-Nan Lee ◽  
Hsueh-Hsiao Wang ◽  
Cheng-Huang Su ◽  
Hsin-I Lee ◽  
Yen-Hung Chou ◽  
...  
Keyword(s):  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Cell Senescence ◽  
Endothelial Progenitor

scholarly journals Coenzyme Q10 Attenuates High Glucose-Induced Endothelial Progenitor Cell Dysfunction through AMP-Activated Protein Kinase Pathways

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Hsiao-Ya Tsai ◽  
Chih-Pei Lin ◽  
Po-Hsun Huang ◽  
Szu-Yuan Li ◽  
Jia-Shiong Chen ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Coenzyme Q10 ◽  
High Glucose ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Heme Oxygenase 1 ◽  
Diabetic Patients ◽  
No Production ◽  
Endothelial Progenitor ◽  
Amp Activated Protein Kinase

Coenzyme Q10 (CoQ10), an antiapoptosis enzyme, is stored in the mitochondria of cells. We investigated whether CoQ10 can attenuate high glucose-induced endothelial progenitor cell (EPC) apoptosis and clarified its mechanism. EPCs were incubated with normal glucose (5 mM) or high glucose (25 mM) enviroment for 3 days, followed by treatment with CoQ10 (10 μM) for 24 hr. Cell proliferation, nitric oxide (NO) production, and JC-1 assay were examined. The specific signal pathways of AMP-activated protein kinase (AMPK), eNOS/Akt, and heme oxygenase-1 (HO-1) were also assessed. High glucose reduced EPC functional activities, including proliferation and migration. Additionally, Akt/eNOS activity and NO production were downregulated in high glucose-stimulated EPCs. Administration of CoQ10 ameliorated high glucose-induced EPC apoptosis, including downregulation of caspase 3, upregulation of Bcl-2, and increase in mitochondrial membrane potential. Furthermore, treatment with CoQ10 reduced reactive oxygen species, enhanced eNOS/Akt activity, and increased HO-1 expression in high glucose-treated EPCs. These effects were negated by administration of AMPK inhibitor. Transplantation of CoQ10-treated EPCs under high glucose conditions into ischemic hindlimbs improved blood flow recovery. CoQ10 reduced high glucose-induced EPC apoptosis and dysfunction through upregulation of eNOS, HO-1 through the AMPK pathway. Our findings provide a potential treatment strategy targeting dysfunctional EPC in diabetic patients.

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