Proangiogenic Tie2+ Macrophages Infiltrate Human and Murine Endometriotic Lesions and Dictate Their Growth in a Mouse Model of the Disease

Capobianco A, Annalisa Capobianco, Monno A, Antonella Monno, Lucia Cottone, Mary Anna Venneri, Daniela Biziato, Biziato D, Di Puppo F, Francesca Di Puppo, Francesca Puppo, Stefano Ferrari, Ferrari S, Michele De Palma, Manfredi AA, Angelo A Manfredi, Patrizia Rovere-Querini, Patrizia Rovere‐Querini, Rovere-Querini P
The American journal of pathology · 2011 · vol. 179(5) , pp. 2651–2659 · doi:10.1016/j.ajpath.2011.07.029 · PMID:21924227 · PMC3204092 · W2135503654
article OA: bronze CC0 ⤵ 68 in-corpus citations
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Proangiogenic Tie2+ macrophages were found to infiltrate both human and mouse endometriotic lesions and to drive lesion growth in a mouse model.

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Abstract

Endometriosis affects women of reproductive age, causing infertility and pain. Although immune cells are recruited in endometriotic lesions, their role is unclear. Tie2-expressing macrophages (TEMs) have nonredundant functions in promoting angiogenesis and growth of experimental tumors. Here we show that human TEMs infiltrate areas surrounding newly formed endometriotic blood vessels. We set up an ad hoc mouse model in which TEMs, and not Tie2-expressing endothelial cells, are targeted. We transplanted in wild-type recipients bone marrow cells expressing a suicide gene (Herpes simplex virus type 1 thymidine kinase) under the Tie2 promoter/enhancer. TEMs infiltrated endometriotic lesions. TEM depletion by ganciclovir administration arrested the growth of established lesions, without toxicity. Lesion architecture was disrupted, with: i) loss of glandular organization, ii) reduced neovascularization, and iii) activation of caspase 3 in CD31(+) endothelial cells. Thus, TEMs are important for maintaining the viability of newly formed vessels and represent a potential therapeutic target in endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Leiomyoma Macrophages Peritoneal Diseases Receptor, TIE-2 Uterine Neoplasms Adult Animals Apoptosis Caspase 3 Caspase 3 Endometriosis Female Hematopoietic Stem Cell Transplantation Hematopoietic Stem Cell Transplantation Humans Leiomyoma Macrophages Macrophages Mice

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