For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
25
views
36
references
 Top references
cited by
5
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      352
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Localization of collagen modifying enzymes on fibroblastic reticular cells and follicular dendritic cells in non-neoplastic and neoplastic lymphoid tissues

      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

          The aim of this study was to evaluate the localization of collagen modifying enzymes (CMEs) on fibroblastic reticular cells (FRCs) and follicular dendritic cells (FDCs) in non-neoplastic lymphoid tissues and various malignant lymphomas. The expression of prolyl 4-hydroxylase 1 (P4H1), lysyl hydroxylase 3 (LH3), and protein disulfide isomerase (PDI) was frequently observed on FRCs and FDCs in the germinal center (GC), except for the mantle zone. The expression of CMEs was lower in most lymphomas than in their respective postulated normal counterparts. The ratio of transglutaminase II + FRCs/CD35 + FDCs was also lower in follicular lymphomas (FL) than in other lymphomas. The mRNAs of some CMEs (P4H1, prolyl 4-hydroxylase 3, LH3, and heat shock protein 47) were confirmed in almost all lymphomas. These results indicate that lymphoma cell proliferation suppresses/decreases the number of CMEs expressing FRCs and FDCs in most lymphomas.

          Related collections

          Most cited references36

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

          Transcriptional profiling of stroma from inflamed and resting lymph nodes defines immunological hallmarks

          Deepali Malhotra, Anne Fletcher, Jillian L. Astarita … (2012)
          Lymph node stromal cells (LNSCs) closely regulate immunity and self-tolerance, yet key aspects of their biology remain poorly illuminated. Comparative transcriptomic analyses of murine LNSC subsets revealed expression of important immune mediators, growth factors, and novel structural components. Pairwise analyses of ligands and cognate receptors across hematopoietic and stromal subsets suggested a complex web of cross-talk. Compared with skin and thymic fibroblasts, fibroblastic reticular cells (FRCs) were enriched in genes relevant to cytokine signaling. LNSCs from inflamed lymph nodes upregulated acute phase response genes, chemokines, and antigen presentation genes. Poorly studied podoplanin−CD31− LNSCs showed similarities to FRCs, but lacked IL-7 expression, and were identified as myofibroblastic integrin α7+ pericytes. Together these data comprehensively describe the transcriptional characteristics of LNSC subsets.
          Article 0 comments Cited 187 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Stromal cell contributions to the homeostasis and functionality of the immune system.

            Scott N. Mueller, Ronald N Germain (2009)
            A defining characteristic of the immune system is the constant movement of many of its constituent cells through the secondary lymphoid tissues, mainly the spleen and lymph nodes, where crucial interactions that underlie homeostatic regulation, peripheral tolerance and the effective development of adaptive immune responses take place. What has only recently been recognized is the role that non-haematopoietic stromal elements have in many aspects of immune cell migration, activation and survival. In this Review, we summarize our current understanding of lymphoid compartment stromal cells, examine their possible heterogeneity, discuss how these cells contribute to immune homeostasis and the efficient initiation of adaptive immune responses, and highlight how targeting of these elements by some pathogens can influence the host immune response.
            Article 0 comments Cited 157 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The tenascin family of ECM glycoproteins: structure, function, and regulation during embryonic development and tissue remodeling.

              F. Jones, P Jones (2000)
              The determination of animal form depends on the coordination of events that lead to the morphological patterning of cells. This epigenetic view of development suggests that embryonic structures arise as a consequence of environmental influences acting on the properties of cells, rather than an unfolding of a completely genetically specified and preexisting invisible pattern. Specialized cells of developing multicellular organisms are surrounded by a complex extracellular matrix (ECM), comprised largely of different collagens, proteoglycans, and glycoproteins. This ECM is a substrate for tissue morphogenesis, lends support and flexibility to mature tissues, and acts as an epigenetic informational entity in the sense that it transduces and integrates intracellular signals via distinct cell surface receptors. Consequently, ECM-receptor interactions have a profound influence on major cellular programs including growth, differentiation, migration, and survival. In contrast to many other ECM proteins, the tenascin (TN) family of glycoproteins (TN-C, TN-R, TN-W, TN-X, and TN-Y) display highly restricted and dynamic patterns of expression in the embryo, particularly during neural development, skeletogenesis, and vasculogenesis. These molecules are reexpressed in the adult during normal processes such as wound healing, nerve regeneration, and tissue involution, and in pathological states including vascular disease, tumorigenesis, and metastasis. In concert with a multitude of associated ECM proteins and cell surface receptors that include members of the integrin family, TN proteins impart contrary cellular functions, depending on their mode of presentation (i.e., soluble or substrate-bound) and the cell types and differentiation states of the target tissues. Expression of tenascins is regulated by a variety of growth factors, cytokines, vasoactive peptides, ECM proteins, and biomechanical factors. The signals generated by these factors converge on particular combinations of cis-regulatory elements within the recently identified TN gene promoters via specific transcriptional activators or repressors. Additional complexity in regulating TN gene expression is achieved through alternative splicing, resulting in variants of TN polypeptides that exhibit different combinations of functional protein domains. In this review, we discuss some of the recent advances in TN biology that provide insights into the complex way in which the ECM is regulated and how it functions to regulate tissue morphogenesis and gene expression. Copyright 2000 Wiley-Liss, Inc.
              Article 0 comments Cited 108 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Leuk Lymphoma
                Journal ID (iso-abbrev): Leuk. Lymphoma
                Journal ID (archive): ILAL
                Journal ID (publisher-id): ilal20
                Title: Leukemia & Lymphoma
                Publisher: Taylor & Francis
                ISSN (Print): 1042-8194
                ISSN (Electronic): 1029-2403
                Publication date (Print): 2 July 2016
                Publication date (Electronic): 24 December 2015
                Volume: 57
                Issue: 7
                Pages: 1687-1696
                Affiliations
                [ a ]Department of Pathological Diagnostics, Yamagata University Faculty of Medicine , Yamagata, Japan
                Author notes
                CONTACT Rintaro Ohe, MD, PhD r-ooe@ 123456med.id.yamagata-u.ac.jp Department of Pathological Diagnostics, Yamagata University Faculty of Medicine , 2-2-2 Iida-Nishi, Yamagata 990-9585, Japan Supplemental data for this article can be accessed http://dx.doi.org/10.3109/10428194.2015.1107907.
                Article
                Publisher ID: 1107907
                DOI: 10.3109/10428194.2015.1107907
                PMC ID: 4926777
                PubMed ID: 26700650
                SO-VID: 4c57f5e7-d2dd-4885-8688-b4d758525139
                Copyright © © 2015 The Author(s). Published by Taylor & Francis
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

                History
                Date received : 20 July 2015
                Date revision received : 5 September 2015
                Date accepted : 10 October 2015
                Page count
                Pages: 10
                Categories
                Subject: Article
                Subject: Original Articles: Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: collagen modifying enzyme,fibroblastic reticular cell,follicular dendritic cell,malignant lymphoma
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: collagen modifying enzyme, fibroblastic reticular cell, follicular dendritic cell, malignant lymphoma

                Comments

                Comment on this article

                scite_

                Similar content352

                See all similar

                Cited by5

                See all cited by

                Most referenced authors296

                See all reference authors