For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
13
views
33
references
 Top references
cited by
36
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      222
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Tissue-resident macrophages promote extracellular matrix homeostasis in the mammary gland stroma of nulliparous mice

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      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

          Tissue-resident macrophages in the mammary gland are found in close association with epithelial structures and within the adipose stroma, and are important for mammary gland development and tissue homeostasis. Macrophages have been linked to ductal development in the virgin mammary gland, but less is known regarding the effects of macrophages on the adipose stroma. Using transcriptional profiling and single-cell RNA sequencing approaches, we identify a distinct resident stromal macrophage subpopulation within the mouse nulliparous mammary gland that is characterized by the expression of Lyve-1, a receptor for the extracellular matrix (ECM) component hyaluronan. This subpopulation is enriched in genes associated with ECM remodeling and is specifically associated with hyaluronan-rich regions within the adipose stroma and fibrous capsule of the virgin mammary gland. Furthermore, macrophage depletion leads to enhanced accumulation of hyaluronan-associated ECM in the adipose-associated stroma, indicating that resident macrophages are important for maintaining homeostasis within the nulliparous mammary gland stroma.

          Related collections

          Most cited references33

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

          Tissue-Resident Macrophage Ontogeny and Homeostasis.

          Florent Ginhoux, Martin Guilliams (2016)
          Defining the origins and developmental pathways of tissue-resident macrophages should help refine our understanding of the role of these cells in various disease settings and enable the design of novel macrophage-targeted therapies. In recent years the long-held belief that macrophage populations in the adult are continuously replenished by monocytes from the bone marrow (BM) has been overturned with the advent of new techniques to dissect cellular ontogeny. The new paradigm suggests that several tissue-resident macrophage populations are seeded during waves of embryonic hematopoiesis and self-maintain independently of BM contribution during adulthood. However, the exact nature of the embryonic progenitors that give rise to adult tissue-resident macrophages is still debated, and the mechanisms enabling macrophage population maintenance in the adult are undefined. Here, we review the emergence of these concepts and discuss current controversies and future directions in macrophage biology.
          Article 0 comments Cited 692 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Leukocyte complexity predicts breast cancer survival and functionally regulates response to chemotherapy.

            David DeNardo, Donal Brennan, Elton Rexhepaj … (2011)
            Immune-regulated pathways influence multiple aspects of cancer development. In this article we demonstrate that both macrophage abundance and T-cell abundance in breast cancer represent prognostic indicators for recurrence-free and overall survival. We provide evidence that response to chemotherapy is in part regulated by these leukocytes; cytotoxic therapies induce mammary epithelial cells to produce monocyte/macrophage recruitment factors, including colony stimulating factor 1 (CSF1) and interleukin-34, which together enhance CSF1 receptor (CSF1R)-dependent macrophage infiltration. Blockade of macrophage recruitment with CSF1R-signaling antagonists, in combination with paclitaxel, improved survival of mammary tumor-bearing mice by slowing primary tumor development and reducing pulmonary metastasis. These improved aspects of mammary carcinogenesis were accompanied by decreased vessel density and appearance of antitumor immune programs fostering tumor suppression in a CD8+ T-cell-dependent manner. These data provide a rationale for targeting macrophage recruitment/response pathways, notably CSF1R, in combination with cytotoxic therapy, and identification of a breast cancer population likely to benefit from this novel therapeutic approach. These findings reveal that response to chemotherapy is in part regulated by the tumor immune microenvironment and that common cytotoxic drugs induce neoplastic cells to produce monocyte/macrophage recruitment factors, which in turn enhance macrophage infiltration into mammary adenocarcinomas. Blockade of pathways mediating macrophage recruitment, in combination with chemotherapy, significantly decreases primary tumor progression, reduces metastasis, and improves survival by CD8+ T-cell-dependent mechanisms, thus indicating that the immune microenvironment of tumors can be reprogrammed to instead foster antitumor immunity and improve response to cytotoxic therapy.
            Article 0 comments Cited 659 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Macrophages: master regulators of inflammation and fibrosis.

              Thomas Wynn, Luke Barron (2010)
              Macrophages are found in close proximity with collagen-producing myofibroblasts and indisputably play a key role in fibrosis. They produce profibrotic mediators that directly activate fibroblasts, including transforming growth factor-beta1 and platelet-derived growth factor, and control extracellular matrix turnover by regulating the balance of various matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases. Macrophages also regulate fibrogenesis by secreting chemokines that recruit fibroblasts and other inflammatory cells. With their potential to act in both a pro- and antifibrotic capacity, as well as their ability to regulate the activation of resident and recruited myofibroblasts, macrophages and the factors they express are integrated into all stages of the fibrotic process. These various, and sometimes opposing, functions may be performed by distinct macrophage subpopulations, the identification of which is a growing focus of fibrosis research. Although collagen-secreting myofibroblasts once were thought of as the master "producers" of fibrosis, this review will illustrate how macrophages function as the master "regulators" of fibrosis. Copyright Thieme Medical Publishers.
              Article 0 comments Cited 457 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Kathryn L Schwertfeger:
                ORCID: https://orcid.org/0000-0002-9755-7774
                Satyajit Rath: Role: Senior Editor
                Carla V Rothlin: Role: Reviewing Editor
                Journal
                Journal ID (nlm-ta): eLife
                Journal ID (iso-abbrev): Elife
                Journal ID (publisher-id): eLife
                Title: eLife
                Publisher: eLife Sciences Publications, Ltd
                ISSN (Electronic): 2050-084X
                Publication date (Electronic, pub): 01 June 2020
                Publication date Collection: 2020
                Volume: 9
                Electronic Location Identifier: e57438
                Affiliations
                [1 ]Department of Laboratory Medicine and Pathology, University of Minnesota MinneapolisUnited States
                [2 ]University of Minnesota Supercomputing Institute, University of Minnesota MinneapolisUnited States
                [3 ]Comparative and Molecular Biosciences Graduate Program, University of Minnesota MinneapolisUnited States
                [4 ]Department of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane School of Medicine New OrleansUnited States
                [5 ]Masonic Cancer Center, University of Minnesota MinneapolisUnited States
                [6 ]Center for Immunology, University of Minnesota MinneapolisUnited States
                Indian Institute of Science Education and Research (IISER) India
                Yale School of Medicine United States
                Yale School of Medicine United States
                The University of Queensland Australia
                Author notes
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-9052-0023
                https://orcid.org/0000-0001-5535-1535
                https://orcid.org/0000-0002-9755-7774
                Article
                Publisher ID: 57438
                DOI: 10.7554/eLife.57438
                PMC ID: 7297528
                PubMed ID: 32479261
                SO-VID: f6dd7269-f329-49fe-a2bf-1fd844468215
                Copyright © © 2020, Wang et al
                License:

                This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

                History
                Date received : 31 March 2020
                Date accepted : 31 May 2020
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: T 32 fellowship, OD010993
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000048, American Cancer Society;
                Award ID: Post-doctoral fellowship, 132570-PF-18-140-01-CSM
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000048, American Cancer Society;
                Award ID: Clinical Scholar Development Grant, 132574-CSDG-18-139-01-CSM
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: R01CA212518
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: R01HD095858
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: R01CA235385
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: R01CA215052
                Award Recipient :
                The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
                Categories
                Subject: Research Article
                Subject: Developmental Biology
                Subject: Immunology and Inflammation
                Custom metadata
                Author impact statement A distinct resident macrophage subpopulation that localizes to the adipose stroma and fibrous capsule of the nulliparous mammary gland and to extracellular matrix-enriched stroma surrounding mammary tumors is identified.

                ScienceOpen disciplines: Life sciences
                Keywords: mammary gland,macrophage,stroma,extracellular matrix,mouse
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: mammary gland, macrophage, stroma, extracellular matrix, mouse

                Comments

                Comment on this article

                scite_

                Similar content222

                See all similar

                Cited by36

                See all cited by

                Most referenced authors1,521

                See all reference authors