Author:
Ono Yosuke,Yoshino Osamu,Hiraoka Takehiro,Sato Erina,Furue Akiko,Nawaz Allah,Hatta Hideki,Fukushi Yoshiyuki,Wada Shinichiro,Tobe Kazuyuki,Hirota Yasushi,Osuga Yutaka,Unno Nobuya,Saito Shigeru
Abstract
AbstractIn endometriosis, M2 MΦs are dominant in endometriotic lesions, but the actual role of M2 MΦ is unclear. CD206 positive (+) MΦ is classified in one of M2 type MΦs and are known to produce cytokines and chemokines. In the present study, we used CD206 diphtheria toxin receptor mice, which enable to deplete CD206+ cells with diphtheria toxin (DT) in an endometriosis mouse model. The depletion of CD206+ MΦ decreased the total weight of endometriotic-like lesions significantly (p < 0.05). In the endometriotic-like lesions in the DT group, a lower proliferation of endometriotic cells and the decrease of angiogenesis were observed. In the lesions, the mRNA levels of VEGFA and TGFβ1, angiogenic factors, in the DT group significantly decreased to approximately 50% and 30% of control, respectively. Immunohistochemical study revealed the expressions of VEGFA and an endothelial cell marker CD31 in lesions of the DT group, were dim compared to those in control. Also, the number of TGFβ1 expressing MΦ was significantly reduced compared to control. These data suggest that CD206+ MΦ promotes the formation of endometriotic-like lesions by inducing angiogenesis around the lesions.
Funder
Health and Labor Sciences Research Grants
The Smoking Research Foundation
Publisher
Springer Science and Business Media LLC
Cited by
22 articles.
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