4.5 Article

Immunosuppressive macrophages induced by IDO1 promote the growth of endometrial stromal cells in endometriosis

Journal

MOLECULAR MEDICINE REPORTS
Volume 15, Issue 4, Pages 2255-2260

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2017.6242

Keywords

endometriosis; indoleamine 2,3-dioxygenase; endometrial stromal cell; macrophage; cell proliferation

Funding

  1. National Natural Science Foundation of China [81601354]
  2. National Science Foundation of Jiangsu Province, China [BK20160128]
  3. Fundamental Research Funds for the Central Universities [021414380180]

Ask authors/readers for more resources

It was previously demonstrated that anomalous expression of indoleamine 2,3-dioxygenase-1 (IDO1) in endometrial stromal cells (ESCs) stimulated an inflammatory response that subsequently initiated the activation of immunosuppressive macrophages in endometriosis. The aim of the present study was to clarify the effect of IDO1-induced macrophages on the growth of ESCs in endometriosis. Normal ESCs, ectopic ESCs and normal ESCs treated with plasmid pEGFP-N1-IDO1 or SD11-IDO1 short hairpin RNA were co-cultured with peripheral blood-derived monocyte (PBMC)-driven macrophages directly for 48 h. Compared with normal ESCs, the PBMC-driven macrophages that were co-cultured with ectopic ESCs displayed a lower phagocytic ability. pEGFP-N1-IDO1 transfection of normal ESCs also decreased the phagocytic ability of co-cultured macrophages. Additionally, pEGFP-N1-IDO1-transfected ESC-induced macrophages significantly increased the viability and proliferation of ESCs, while ESC apoptosis was decreased, compared with control ESCs. In conclusion, IDO1 educated-macrophages may facilitate the survival of retrograde endometrial tissues, and be involved in the pathogenesis of endometriosis.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.5
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available