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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Diabetes+Res
2016 ; 2016
(ä): 6384759
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Coenzyme Q10 Attenuates High Glucose-Induced Endothelial Progenitor Cell
Dysfunction through AMP-Activated Protein Kinase Pathways
#MMPMID26682233
Tsai HY
; Lin CP
; Huang PH
; Li SY
; Chen JS
; Lin FY
; Chen JW
; Lin SJ
J Diabetes Res
2016[]; 2016
(ä): 6384759
PMID26682233
show ga
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) environment for
3 days, followed by treatment with CoQ10 (10 ?M) 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.