Chronic hyperuricemia impairs blood flow recovery in the ischemic hindlimb through suppression of endothelial progenitor cells
Journal
Oncotarget
Journal Volume
9
Journal Issue
10
Pages
9285-9298
Date Issued
2018
Author(s)
Chen I.-C.
Kuo C.-S.
Tsai H.-Y.
Lin C.-P.
Li S.-Y.
Chou R.-H.
Huang P.-H.
Chen J.-W.
Lin S.-J.
Abstract
OBJECTIVE: Chronic hyperuricemia is associated with cardiovascular disease, but its impact on endothelial progenitor cells (EPC) and ischemia-induced neovascularization remains unclear. Herein we investigated whether chronic hyperuricemia could impede blood flow recovery in response to tissue ischemia by suppression of EPC. METHODS: ). RESULTS: Incubation with a high-level uric acid medium (10 mg/dL) significantly suppressed EPC proliferation, reduced NO production, and lessened phosphorylation of Akt and eNOS. Moreover, EPC treated with high-level uric acid increased reactive oxygen species production, promoted cellular apoptosis and senescence, and also inhibited EPC tube formation. Four weeks after hindlimb ischemia surgery, the chronic hyperuricemia mice had significantly reduced tissue reperfusion, EPC mobilization, and impaired neovascularization in the ischemic hindlimbs compared with the control mice. CONCLUSIONS: Chronic hyperuricemia impaired blood flow recovery and EPC mobilization in response to tissue ischemia, and these effects could have occurred through suppression of EPC.
SDGs
Publisher
Impact Journals LLC
Type
journal article