Abstract
Peripheral vascular disease usually leads to vascular injury and inflammatory reaction, and the main therapeutic measures are improving angiogenesis and restoring blood flow. Interleukin-33 (IL-33) is a pleiotropic cytokine implicated in immune responses and tissue repair. Here, we explore the effect of IL-33 in hindlimb ischemic injury and elucidate the potential mechanisms of action. The expression of IL-33 and its receptor ST2 were obviously elevated in ischemic hindlimb of mice underwent ligation surgery. Exogenous IL-33 apparently facilitated blood flow restoration in ischemic hindlimb, whereas ST2-deficient mice displayed severe defects in ischemic hindlimb repair. The activation of IL-33/ST2 signaling contributed to revascularization in ischemic hindlimb, which was related to modulation of proangiogenic function of endothelial cells. Further ex vivo and in vitro studies revealed that IL-33 clearly accelerated angiogenesis by Matrigel plug and tube formation assays. Mechanically, the angiogenic function of IL-33 is involved in regulation of Akt/eNOS pathway. All together, these findings imply that IL-33-mediated endothelial angiogenesis may represent a prospective effective therapy for hindlimb ischemic damage.
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