14
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      CD11c+ M1-like macrophages (MΦs) but not CD206+ M2-like MΦ are involved in folliculogenesis in mice ovary

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Macrophages (MΦs) are involved in folliculogenesis and ovulation. However, it is unknown which type of MΦ, M1 or M2, plays a more essential role in the ovary. CD206 or CD11c diphtheria toxin receptor transgenic (DTR) mice, which enable depletion of CD206+ M2 MΦs and CD11c+ MΦ or CD11c+ Dendritic cells (DCs), respectively, were used. Oocytes were used for in vitro fertilization and embryo transfer. In vitro fertilized embryos derived from M2 MΦ depleted oocytes were transferred to pseudo pregnant wild type mice. CD11c DTR mice were also used to investigate the role of CD11c cells, M1 MΦ and DCs in folliculogenesis. In WT mice, the proportion of CD206+ M2-like MΦs was not increased in follicular induction, while that of CD11c+ M1-like MΦs was increased. In CD206 DTR mice, folliculogenesis was normal and the ovulation number, fertilization rate, and implantation rate were similar to those in WT mice. In CD11c DTR mice, folliculogenesis was impaired with ovarian hemorrhage and the staining of platelet derived growth factor-receptor β (PDGF-Rβ), a marker of pericytes, and CD34, a marker of endothelial cells, was reduced. CD11c+ cells, M1 MΦs or DCs, may be involved in folliculogenesis, while M2 MΦs are not involved in folliculogenesis.

          Related collections

          Most cited references39

          • Record: found
          • Abstract: found
          • Article: not found

          Mice deficient for PDGF B show renal, cardiovascular, and hematological abnormalities.

          Platelet-derived growth factor (PDGF) affects the growth, migration, and function in vitro of mesenchymal cells, but little is known about its normal physiological functions in vivo. We show here that mice deficient for PDGF B die perinatally and display several anatomical and histological abnormalities. Kidney glomerular tufts do not form, apparently because of absence of mesangial cells. Instead, a single or a few distended capillary loops fill the glomerular space. The heart and some large arteries dilate in late-stage embryos. Most PDGF B mutant embryos develop fatal hemorrhages just prior to birth. Their hematological status includes erythroblastosis, macrocytic anemia, and thrombocytopenia. On the basis of these findings, we conclude that PDGF B has crucial roles in vivo in establishing certain renal and circulatory functions.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Macrophage contributions to ovarian function.

            Macrophages are multifunctional cells that play key roles in the immune response and are abundant throughout female reproductive tissues. Macrophages are identified in tissues by their expression of cell surface receptors and can execute diverse functional activities, including phagocytosis and degradation of foreign antigens, matrix dissolution and tissue remodelling, and production and secretion of cytokines, chemokines and growth factors. Their specific localization and variations in distribution in the ovary during different stages of the cycle, as well as their presence in peri-ovulatory human follicular fluid, suggest that macrophages play diverse roles in intra-ovarian events including folliculogenesis, tissue restructuring at ovulation and corpus luteum formation and regression. This review presents the existing evidence for the regulation of ovarian function by macrophages and macrophage-derived products, highlighting the implications of these cells in ovarian diseases, particularly polycystic ovary syndrome, endometriosis and premature ovarian failure.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Macrophages regulate corpus luteum development during embryo implantation in mice.

              Macrophages are prominent in the uterus and ovary at conception. Here we utilize the Cd11b-Dtr mouse model of acute macrophage depletion to define the essential role of macrophages in early pregnancy. Macrophage depletion after conception caused embryo implantation arrest associated with diminished plasma progesterone and poor uterine receptivity. Implantation failure was alleviated by administration of bone marrow-derived CD11b+F4/80+ monocytes/macrophages. In the ovaries of macrophage-depleted mice, corpora lutea were profoundly abnormal, with elevated Ptgs2, Hif1a, and other inflammation and apoptosis genes and with diminished expression of steroidogenesis genes Star, Cyp11a1, and Hsd3b1. Infertility was rescued by exogenous progesterone, which confirmed that uterine refractoriness was fully attributable to the underlying luteal defect. In normally developing corpora lutea, macrophages were intimately juxtaposed with endothelial cells and expressed the proangiogenic marker TIE2. After macrophage depletion, substantial disruption of the luteal microvascular network occurred and was associated with altered ovarian expression of genes that encode vascular endothelial growth factors. These data indicate a critical role for macrophages in supporting the extensive vascular network required for corpus luteum integrity and production of progesterone essential for establishing pregnancy. Our findings raise the prospect that disruption of macrophage-endothelial cell interactions underpinning corpus luteum development contributes to infertility in women in whom luteal insufficiency is implicated.
                Bookmark

                Author and article information

                Contributors
                kawotan-tky@umin.ac.jp
                yutakaos-tky@umin.ac.jp
                s30saito@med.u-toyama.ac.jp
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                25 May 2018
                25 May 2018
                2018
                : 8
                : 8171
                Affiliations
                [1 ]ISNI 0000 0001 2171 836X, GRID grid.267346.2, Department of Obstetrics and Gynecology, , University of Toyama, ; Toyama, Japan
                [2 ]ISNI 0000 0001 2151 536X, GRID grid.26999.3d, Department of Obstetrics and Gynecology, , University of Tokyo, ; Tokyo, Japan
                [3 ]ISNI 0000 0001 2171 836X, GRID grid.267346.2, First Department of Internal Medicine, , University of Toyama, ; Toyama, Japan
                [4 ]ISNI 0000 0001 2171 836X, GRID grid.267346.2, Department of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Sciences, , University of Toyama, ; Toyama, Japan
                [5 ]ISNI 0000 0001 2171 836X, GRID grid.267346.2, Division of Animal Resources and Development, , University of Toyama, ; Toyama, Japan
                Author information
                http://orcid.org/0000-0002-4546-1084
                Article
                25837
                10.1038/s41598-018-25837-3
                5970206
                29802255
                b7652e81-f9ca-414d-9f8d-d9d1644975e5
                © The Author(s) 2018

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 14 November 2017
                : 20 April 2018
                Categories
                Article
                Custom metadata
                © The Author(s) 2018

                Uncategorized
                Uncategorized

                Comments

                Comment on this article