Prevention of inflammatory angiogenesis is critical for suppressing chronic inflammation and inhibiting inflammatory tissue damage. Angiogenesis is particularly detrimental to the cornea as pathological growth of new blood vessels can lead to marked vision impairment and even loss of vision. The expression of pro-inflammatory cytokines by injured tissues has been shown to exacerbate the inflammatory cascade, including angiogenesis. Interleukin 36 cytokine, a subfamily of the Interleukin 1 superfamily, consists of three pro-inflammatory agonists IL36α, IL36β, and IL36γ and an IL36 receptor antagonist (IL36Ra). Our data show that human vascular endothelial cells constitutively express the cognate receptor IL36R.

Moreover, the current investigation, for the first time, characterizes the direct contribution of IL36γ to various angiogenic processes. IL36γ upregulates the expression of vascular endothelial growth factors (VEGFs) and their receptors VEGFR2 and VEGFR3 by human vascular endothelial cells, suggesting IL36γ mediates the VEGF-VEGFR signaling by endothelial cells. Moreover, by utilizing a naturally occurring antagonist IL36Ra in a murine model of inflammatory angiogenesis, the current study demonstrates that blockade of endogenous IL36γ signaling results in significant retardation of inflammatory angiogenesis. The current investigation on the pro-angiogenic function of IL36γ provides novel evidence for the development of IL36γ-targeting strategies to hamper inflammatory angiogenesis.

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Mishita
Jornal co-ordinator
Journal of Heart and Cardiovascular Research