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

      1 , 2 , 1
      Molecular medicine reports
      Spandidos Publications

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          Abstract

          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.

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          Author and article information

          Journal
          Mol Med Rep
          Molecular medicine reports
          Spandidos Publications
          1791-3004
          1791-2997
          Apr 2017
          : 15
          : 4
          Affiliations
          [1 ] Reproductive Medicine Center, Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, P.R. China.
          [2 ] Hospital and Institute of Obstetrics and Gynecology, Shanghai Medical School, Fudan University, Shanghai 200011, P.R. China.
          Article
          10.3892/mmr.2017.6242
          28260094
          fdc53561-d370-43ef-a128-a715d9913d39
          History

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