TSP1‐CD47‐SIRPα signaling facilitates the development of endometriosis by mediating the survival of ectopic endometrium

Yukai Liu, Ming‐Qing Li, Chunyan Wei, Lingli Tang, Yan‐Ran Sheng, Yanran Sheng, Yuyin Liu, Da‐Jin Li, Ding Ding, Jianping Qiu, Xiao‐Yong Zhu
American journal of reproductive immunology (New York, N.Y. : 1989) · 2020 · vol. 83(6) , pp. e13236 · doi:10.1111/aji.13236 · PMID:32196807 · W3012444781
article OA: closed CC0 ⤵ 15 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

Thrombospondin-1 (TSP1) binding to CD47 on endometrial cells enhances their survival and promotes endometriosis development by suppressing macrophage phagocytosis and boosting angiogenesis, effects counteracted by CD47 blockade.

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Abstract

PROBLEM: To explore whether the thrombospondin-1(TSP1)-CD47-signal regulatory protein alpha (SIRPα) signaling pathway has impacts on the development of endometriosis. METHOD OF STUDY: Endometrial stromal cells (ESCs) originated from ectopic and eutopic endometrial tissues with or without endometriosis. Monocytes (Macrophages) were isolated from peripheral blood and peritoneal fluids with or without endometriosis. The expression levels of molecules were investigated by flow cytometry (FCM), immunohistochemistry (IHC), and RT-qPCR. The concentration of TSP1 was assessed via ELISA. The capacities of angiogenesis and phagocytosis were measured via tube formation assay and phagocytic assay, respectively. RESULTS: We confirmed the up-regulation of critical molecules within the pathway in endometriosis patients. TSP1 can encourage normal ESCs (NESCs) growth and fibrosis. It simultaneously promotes the secretion of inflammatory factors and inhibits the phagocytic abilities of macrophages. Moreover, the proliferation of vascular endothelial cells (VECs) may be improved by TSP1. These effects may be offset by CD47 blocking antibodies. In addition, ectopic ESCs (EESCs) directly improve SIRPα expression on macrophages, which may further exhaust their phagocytic ability. Phagocytosis efficiency of macrophages on EESCs significantly improves by blocking CD47-SIRPα pathway. CONCLUSION: TSP1-CD47-SIRPα signaling pathway not only improves the viability of NESCs per se but also promotes their survival circumstances by affecting the function of macrophages and VECs, which are mutually reinforcing and jointly promote the development of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Antigens, Differentiation CD47 Antigen Choristoma Endometriosis Endometrium Endothelium, Vascular Receptors, Immunologic Thrombospondin 1 Adult Antibodies, Blocking Antibodies, Blocking Antigens, Differentiation CD47 Antigen CD47 Antigen Cells, Cultured Cell Survival Choristoma Endometriosis Endometriosis Endometrium

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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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