Blocking IL-22, a potential treatment strategy for adenomyosis by inhibiting crosstalk between vascular endothelial and endometrial stromal cells.

Wen-Qing Shang, Jiajun Yu, Jia-Jun Yu, Lei Zhu, Wen-Jie Zhou, Wen‐Jie Zhou, Kai‐Kai Chang, Kai-Kai Chang, Qing Wang, Ming‐Qing Li, Ming-Qing Li
American journal of translational research · 2015 · vol. 7(10) , pp. 1782–97 · PMID:26692924 · W2220013957
article OA: green CC0 ⤵ 7 in-corpus citations
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Interleukin-22 from adenomyosis endometrial stromal cells promotes vascular endothelial cell viability and angiogenesis, which in turn stimulates stromal cell proliferation, suggesting IL-22 blockade as a potential treatment.

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Abstract

Our previous work has demonstrated that interleukin-22 (IL-22) enhances the invasiveness of endometrial stromal cells (ESCs) of adenomyosis in an autocrine manner. In the present study, we further investigated whether IL-22 mediated crosstalk between vascular endothelial cells (VECs) and ESCs in vitro. Here we found that VECs in ectopic lesion from women with adenomyosis highly expressed IL-22 receptors IL-22R1 and IL-10R2. Both recombinant human IL-22 (rhIL-22) and IL-22 from ESCs increased IL-22R1 and IL-10R2 expression on human umbilical vein endothelial cells (HUVECs). Treatment with rhIL-22 led to an elevation of HUVECs viability, but did not influence HUVECs apoptosis. In contrast, anti-human IL-22 neutralizing antibody (α-IL-22) inhibited HUVECs viability induced by supernatants of ESCs. Stimulation with rhIL-22 or ESCs up-regulated CD105 expression on HUVECs and promoted angiogenesis, and α-IL-22 could reverse these effect induced by ESC. Compared to non-treated HUVECs, HUVECs educated by rh-IL-22 or ESCs could further up-regulate Ki-67 and proliferating cell nuclear antigen (PCNA) expression, and down-regulate Fas ligand (FasL) expression in ESCs. However, these effects induced by ESC-educated HUVECs were inhibited by α-IL-22. These results suggest that IL-22 derived from ESC promotes IL-22 receptors expression and enhances the viability, activation and angiogenesis of HUVEC. In turn, the educated HUVEC may further stimulate proliferation and restricts apoptosis of ESC. The integral effect may contribute to the progress of adenomyosis. Blocking IL-22 can disturb crosstalk between ESC and VEC mediated by IL-22, suggesting that blocking IL-22 may be a potential treatment strategy for adenomyosis.

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adenomyosis

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