BACKGROUND: Interleukin (IL)-13, which is a cytokine produced by type 2 helper T cells, has pathophysiological roles in allergic inflammation and fibrosis formation. IL-13 shares many functional properties with IL-4, which is known to inhibit angiogenesis. METHODS AND RESULTS: The effects of IL-13 on angiogenesis were examined using human coronary artery endothelial cells (HCAECs), in addition to investigating the mechanism(s) of this action. Using an in vitro assay of angiogenesis it was demonstrated that IL-13, as well as IL-4, significantly inhibited capillary-like tube formation. Migration of HCAECs, considered to be a process of new capillary tube formation, was also significantly inhibited by IL-13. IL-13 activated signal transduction and transcription 6 (STAT6) as a result of the activation of Janus kinase 2 (JAK2). The inhibitory effect of IL-13 on angiogenesis was abolished by depletion of JAK2 and STAT6 by RNA interference. CONCLUSION: IL-13 has anti-angiogenic activity as a result of activation of JAK2 and subsequent activation of STAT6.
BACKGROUND:Interleukin (IL)-13, which is a cytokine produced by type 2 helper T cells, has pathophysiological roles in allergic inflammation and fibrosis formation. IL-13 shares many functional properties with IL-4, which is known to inhibit angiogenesis. METHODS AND RESULTS: The effects of IL-13 on angiogenesis were examined using human coronary artery endothelial cells (HCAECs), in addition to investigating the mechanism(s) of this action. Using an in vitro assay of angiogenesis it was demonstrated that IL-13, as well as IL-4, significantly inhibited capillary-like tube formation. Migration of HCAECs, considered to be a process of new capillary tube formation, was also significantly inhibited by IL-13. IL-13 activated signal transduction and transcription 6 (STAT6) as a result of the activation of Janus kinase 2 (JAK2). The inhibitory effect of IL-13 on angiogenesis was abolished by depletion of JAK2 and STAT6 by RNA interference. CONCLUSION:IL-13 has anti-angiogenic activity as a result of activation of JAK2 and subsequent activation of STAT6.
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