| First Author | Ono Y | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 853 |
| PubMed ID | 33441630 | Mgi Jnum | J:301657 |
| Mgi Id | MGI:6502285 | Doi | 10.1038/s41598-020-79578-3 |
| Citation | Ono Y, et al. (2021) CD206+ macrophage is an accelerator of endometriotic-like lesion via promoting angiogenesis in the endometriosis mouse model. Sci Rep 11(1):853 |
| abstractText | In endometriosis, M2 MPhis are dominant in endometriotic lesions, but the actual role of M2 MPhi is unclear. CD206 positive (+) MPhi is classified in one of M2 type MPhis 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+ MPhi 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 TGFbeta1, 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 TGFbeta1 expressing MPhi was significantly reduced compared to control. These data suggest that CD206+ MPhi promotes the formation of endometriotic-like lesions by inducing angiogenesis around the lesions. |
