English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

We hypothesized that dipeptidyl peptidase-IV (DPP4) may impair angiogenesis, endothelial function, and the circulating number of endothelial progenitor cells (EPC) in a model of critical limb ischemia (CLI) through ligating the left femoral artery using DPP4-deficient rats.    Methods  Adult male DPP4-deficient (DPP4 D ) rats ( n  = 18) were equally divided into CLI only (DPP4 D -CLI) and CLI treated by granulocyte colony-stimulating factor (GCSF) (DPP4 D -CLI-GCSF). For comparison, age-matched wild-type (WT) Fischer 344 rats ( n  = 18) were randomized into two groups receiving identical treatment compared to their DPP4-deficient counterparts and labeled as WT-CLI ( n  = 9) and WT-CLI-GCSF ( n  = 9), respectively.    Results  The circulating number of EPCs (CD31+, CD34+, CD133, C-kit+) was significantly lower in DPP4-deficient than in WT rats on post-CLI days 1 and 4 (all  P  < 0.01). The ratio of ischemia/normal blood flow was remarkably lower in DPP4 D -CLI-GCSF rats than in WT-CLI-GCSF animals on post-CLI Day 14 (all  P  < 0.01). Protein expressions of pro-angiogenic factors (endothelial nitric oxide synthase (eNOS), CXCR4, SDF-1α, vascular endothelial growth factor (VEGF)) were remarkably higher in WT-CLI than in DPP4 D -CLI rats, and higher in WT-CLI-GCSF than in DPP4 D -CLI-GCSF animals (all  P  < 0.01). Moreover, the numbers of small vessel in the ischemic area were substantially higher in WT-CLI-GCSF than in DPP4 D -CLI-GCSF rats ( P  < 0.001). Furthermore, vasorelaxation and nitric oxide production of the normal femoral artery were significantly reduced in DPP4-deficient than in WT Fischer rats (all  P  < 0.01).    Conclusions  Contrary to our hypothesis, DPP4-deficient rats were inferior to age-matched WT Fischer rats in terms of angiogenesis, endothelial function, circulating EPC number and response to GCSF, suggesting a positive role of DPP4 in maintaining vascular function and tissue perfusion in this experimental setting.

stem cell research and therapy

Paradoxical impairment of angiogenesis, endothelial function and circulating number of endothelial progenitor cells in DPP4-deficient rat after critical limb ischemia