Hypoxia-induced Semaphorin 3A promotes the development of endometriosis through regulating macrophage polarization

Ruyu Yang, Fan Yang, Yajing Wei, Biqi Huang, Tiefeng Cao, Hao Tan, Duo Liu, Qiuyu Zou, Jinjuan Wen, Lei Wen, Xi Lu, Changyang Yu, Heng Cai, Xiaofei Xie, Shaoru Jiang, Shuzhong Yao, Yanchun Liang
International immunopharmacology · 2024 · vol. 138 , pp. 112559 · doi:10.1016/j.intimp.2024.112559 · PMID:38955028 · W4400184506
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Hypoxia-induced Semaphorin 3A, regulated by HIF-1α, promotes endometriosis development by enhancing ESC proliferation and polarization of macrophages towards an anti-inflammatory phenotype.

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Abstract

BACKGROUND: Semaphorin 3A (Sema3A) is a member of neural guidance factor family well-known for inducing the collapse of nerve cell growth cone and regulating nerve redistribution. It also has been characterized as an immunoregulatory and tumor promoting factor. Our previous study showed that Sema3A was involved in the regulation of sympathetic innervation and neuropathic pain of endometriosis. Nevertheless, the role of Sema3A in the development of endometriosis and its potential upstreaming factor are still not clear. METHODS: Histology experiments were carried to detect the expression of Sema3A, hypoxia -inducible factor 1α (HIF-1α) and the distribution of macrophages. Cell experiments were used to explore the effect of Sema3A on the proliferation and migration of endometrial stromal cells (ESCs) and to confirm the regulatory action of HIF-1α on Sema3A. In vivo experiments were carried out to explore the role of Sema3A on the development of endometriosis. RESULTS: Sema3A was highly expressed in endometriotic lesions and could enhanced the proliferation and migration abilities of ESCs. Aberrant macrophage distribution was found in endometriotic lesions. Sema3A also promoted the differentiation of monocytes into anti-inflammatory macrophages, so indirectly mediating the proliferation and migration of ESCs. Hypoxic microenvironment induced Sema3A mRNA and protein expression in ESCs via HIF-1α. Administration of Sema3A promoted the development of endometriosis in a mouse model. CONCLUSIONS: Sema3A, which is regulated by HIF-1α, is a promoting factor for the development of endometriosis. Targeting Sema3A may be a potential treatment strategy to control endometriotic lesions.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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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. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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