AgeR deletion decreases soluble fms-like tyrosine kinase 1 production and improves post-ischemic angiogenesis in uremic
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AgeR deletion decreases soluble fms‑like tyrosine kinase 1 production and improves post‑ischemic angiogenesis in uremic mice Vincent Dupont1,2,3 · Rida Al‑Rifai3 · Gael Poitevin3 · Jeremy Ortillon2 · Laura Jayyosi3 · Christine Terryn4 · Caroline Francois3 · Philippe Rieu1 · Günter Fritz5 · Camile Boulagnon‑Rombi6 · Caroline Fichel6 · Ann Marie Schmidt7 · Claire Tournois3 · Philippe Nguyen3 · Fatouma Touré8,9 Received: 14 April 2020 / Accepted: 17 September 2020 © Springer Nature B.V. 2020
Abstract Peripheral arterial disease occurs more frequently and has a worse prognosis in patients with chronic kidney disease (CKD). The receptor for advanced glycation end products (RAGE) is involved in multiple aspects of uremia-associated vasculopathy. Previous data suggest that the RAGE pathway may promote soluble fms-like tyrosine kinase 1 (sFlt1) production, an antiangiogenic molecule. Thus, we tested the hypothesis that the deletion of AgeR would decrease sFlt1 production and improve post-ischemic revascularization in uremic condition. We used a well-established CKD model (5/6 nephrectomy) in WT and AgeR−/− C57/Bl6 mice. Hindlimb ischemia was induced by femoral artery ligation. Revascularization was evaluated by complementary approaches: ischemic limb retraction, LASCA imagery, and capillary density. The production of sFlt1 was assessed at both RNA and protein levels. After hindlimb ischemia, uremic mice showed slower functional recovery (p
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