Interleukin-37b inhibits the growth of murine endometriosis-like lesions by regulating proliferation, invasion, angiogenesis and inflammation

Yongpei He, He Y, Ting Xiong, Fang Guo, Guo F, Du Z, Zhenzhen Du, Yixian Fan, Fan Y, Huanhuan Sun, Sun H, Feng Zuohua, Feng Z, Zuohua Feng, Guimei Zhang, Zhang G
Molecular human reproduction · 2020 · vol. 26(4) , pp. 240–255 · doi:10.1093/molehr/gaaa014 · PMID:32119739 · W3010618770
Lab / animal OA: bronze CC0 ⤵ 5 in-corpus citations
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Interleukin-37b administration inhibited murine endometriosis-like lesion growth by reducing proliferation, invasion, angiogenesis, and inflammation via the Akt and Erk1/2 signaling pathways.

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Abstract

Endometriosis is a gynecological disease with abnormal expression of interleukin (IL)-37 which can suppress inflammation and the immune system. Here we investigated the role of the IL-37b splice variant in endometriosis in vivo and in vitro. In a murine model of endometriosis, in vivo administration of IL-37b significantly inhibited the development of lesions judged by the number (P = 0.0213), size (P = 0.0130) and weight (P = 0.0152) of lesions. IL-37b had no effect on the early stage of lesion formation, however administration in the growth stage of lesions decreased the number (P = 0.0158), size (P = 0.0158) and weight (P = 0.0258) of lesions compared with PBS control, an effect that was not reversed by macrophage depletion. Expressions of inflammatory factors, matrix metalloproteinases and vascular endothelial growth factor-A mRNA/protein were significantly inhibited in ectopic lesions following IL-37b administration, and in uterine segments treated in vitro. In vitro treatment of uterine segments with IL-37b inhibited phosphorylation of Akt and Erk1/2 in uterine segments. Isolated mouse endometrial stromal treated with IL-37b and transfected with pIL-37b plasmid got suppressed cell proliferation, invasion, angiogenesis and the expression of inflammatory factors. In addition, transfection with pIL-37b significantly decreased the phosphorylation of Akt and Erk1/2. IL-37b also inhibited proliferation and the expression of inflammatory and angiogenesis factors in epithelial cell line RL95-2. These findings suggest that IL-37b may inhibit the growth of lesions by regulating proliferation, invasion, angiogenesis and inflammation through Akt and Erk1/2 signaling pathway.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Interleukin-1 Animals Animals Cell Proliferation Cell Proliferation Cell Proliferation Disease Models, Animal Disease Models, Animal Endometriosis Endometriosis Endometriosis Female Female Inflammation Inflammation Inflammation Interleukin-1 Interleukin-1 Macrophages, Peritoneal

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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Cited by (6)

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