Interleukin-22 receptor 1 upregulation and activation in hypoxic endothelial cells improves perfusion recovery in experimental peripheral arterial disease.

OBJECTIVE:Inflammation induced by muscle ischemia is involved in tissue repair and perfusion recovery in peripheral arterial disease patients. Interleukin (IL)-22 is an inflammatory cytokine discovered in recent years and shows versatile functions; however, its role in remains unknown. Here, we test whether IL-22 and its receptors are involved in angiogenesis in experimental AND RESULTS:Both IL-22 and its receptor-IL-22 receptor 1(IL-22R1) were upregulated in muscle and endothelial cells after ischemia. In experimental duanyu1563 models, blocking IL-22 using IL-22 monoclonal antibody impaired perfusion recovery and angiogenesis; on the other hand, IL-22 treatment improved perfusion recovery. Ischemic muscle tissue was harvested 3 days after experimental duanyu1563 for biochemical test, IL-22 antagonism resulted in decreased Signal Transducer and Activator of Transcription phosphorylation, but did not alter the levels of VEGF-A or cyclic guanine monophosphate (cGMP) levels in ischemic muscle. In cultured endothelial cells, IL-22R1 was upregulated under simulated ischemic conditions, and IL-22 treatment increased phosphorylation, endothelial cell survival and tube formation. Knock down of IL-22R1 or treatment with duanyu18133 inhibitor blunted IL-22-induced endothelial cell survival or tube formation. CONCULSION:Ischemia-induced IL-22 and IL-22R1 upregulation improves angiogenesis in duanyu1563 by inducing duanyu18133 phosphorylation in endothelial cells. IL-22R1 may serve as a new therapeutic target for

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