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      Matrisome Profiling During Intervertebral Disc Development And Ageing

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          Abstract

          Intervertebral disc (IVD) degeneration is often the cause of low back pain. Degeneration occurs with age and is accompanied by extracellular matrix (ECM) depletion, culminating in nucleus pulpous (NP) extrusion and IVD destruction. The changes that occur in the disc with age have been under investigation. However, a thorough study of ECM profiling is needed, to better understand IVD development and age-associated degeneration. As so, iTRAQ LC-MS/MS analysis of foetus, young and old bovine NPs, was performed to define the NP matrisome. The enrichment of Collagen XII and XIV in foetus, Fibronectin and Prolargin in elder NPs and Collagen XI in young ones was independently validated. This study provides the first matrisome database of healthy discs during development and ageing, which is key to determine the pathways and processes that maintain disc homeostasis. The factors identified may help to explain age-associated IVD degeneration or constitute putative effectors for disc regeneration.

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          The Proteomics Identifications (PRIDE) database and associated tools: status in 2013

          Juan Antonio Vizcaíno, Richard Côté, Attila Csordas … (2012)
          The PRoteomics IDEntifications (PRIDE, http://www.ebi.ac.uk/pride) database at the European Bioinformatics Institute is one of the most prominent data repositories of mass spectrometry (MS)-based proteomics data. Here, we summarize recent developments in the PRIDE database and related tools. First, we provide up-to-date statistics in data content, splitting the figures by groups of organisms and species, including peptide and protein identifications, and post-translational modifications. We then describe the tools that are part of the PRIDE submission pipeline, especially the recently developed PRIDE Converter 2 (new submission tool) and PRIDE Inspector (visualization and analysis tool). We also give an update about the integration of PRIDE with other MS proteomics resources in the context of the ProteomeXchange consortium. Finally, we briefly review the quality control efforts that are ongoing at present and outline our future plans.
          Article 0 comments Cited 769 times – based on 0 reviews     Review now
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            What is intervertebral disc degeneration, and what causes it?

            Michael A. Adams, Peter J. Roughley (2006)
            Review and reinterpretation of existing literature. To suggest how intervertebral disc degeneration might be distinguished from the physiologic processes of growth, aging, healing, and adaptive remodeling. The research literature concerning disc degeneration is particularly diverse, and there are no accepted definitions to guide biomedical research, or medicolegal practice. The process of disc degeneration is an aberrant, cell-mediated response to progressive structural failure. A degenerate disc is one with structural failure combined with accelerated or advanced signs of aging. Early degenerative changes should refer to accelerated age-related changes in a structurally intact disc. Degenerative disc disease should be applied to a degenerate disc that is also painful. Structural defects such as endplate fracture, radial fissures, and herniation are easily detected, unambiguous markers of impaired disc function. They are not inevitable with age and are more closely related to pain than any other feature of aging discs. Structural failure is irreversible because adult discs have limited healing potential. It also progresses by physical and biologic mechanisms, and, therefore, is a suitable marker for a degenerative process. Biologic progression occurs because structural failure uncouples the local mechanical environment of disc cells from the overall loading of the disc, so that disc cell responses can be inappropriate or "aberrant." Animal models confirm that cell-mediated changes always follow structural failure caused by trauma. This definition of disc degeneration simplifies the issue of causality: excessive mechanical loading disrupts a disc's structure and precipitates a cascade of cell-mediated responses, leading to further disruption. Underlying causes of disc degeneration include genetic inheritance, age, inadequate metabolite transport, and loading history, all of which can weaken discs to such an extent that structural failure occurs during the activities of daily living. The other closely related definitions help to distinguish between degenerate and injured discs, and between discs that are and are not painful.
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              Integrin-TGF-beta crosstalk in fibrosis, cancer and wound healing.

              Coert Margadant, Arnoud Sonnenberg (2010)
              Accumulating evidence indicates that there is extensive crosstalk between integrins and TGF-beta signalling. TGF-beta affects integrin-mediated cell adhesion and migration by regulating the expression of integrins, their ligands and integrin-associated proteins. Conversely, several integrins directly control TGF-beta activation. In addition, a number of integrins can interfere with both Smad-dependent and Smad-independent TGF-beta signalling in different ways, including the regulation of the expression of TGF-beta signalling pathway components, the physical association of integrins with TGF-beta receptors and the modulation of downstream effectors. Reciprocal TGF-beta-integrin signalling is implicated in normal physiology, as well as in a variety of pathological processes including systemic sclerosis, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease and cancer; thus, integrins could provide attractive therapeutic targets to interfere with TGF-beta signalling in these processes.
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                Author and article information

                Contributors
                Joana Caldeira: joana.caldeira@ineb.up.pt
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 14 September 2017
                Publication date PMC-release: 14 September 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 11629
                Affiliations
                [1 ]ISNI 0000 0001 1503 7226, GRID grid.5808.5, i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, ; Porto, Portugal
                [2 ]ISNI 0000 0001 1503 7226, GRID grid.5808.5, INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Rua Alfredo Allen, 208, ; 4200-180 Porto, Portugal
                [3 ]ISNI 0000 0001 1503 7226, GRID grid.5808.5, IPATIMUP - Institute of Molecular Pathology and Immunology, University of Porto, Rua Júlio Amaral de Carvalho, 45, ; 4200-135 Porto, Portugal
                [4 ]ISNI 0000 0000 9511 4342, GRID grid.8051.c, III – Institute for Interdisciplinary Research, University of Coimbra, Casa Costa Alemão – Pólo II, Rua Dom Francisco de Lemos, ; 3030-789 Coimbra, Portugal
                [5 ]ISNI 0000 0000 9511 4342, GRID grid.8051.c, CNC – Center for Neuroscience and Cell Biology, University of Coimbra, ; 3004-504 Coimbra, Portugal
                [6 ]ISNI 0000 0001 1503 7226, GRID grid.5808.5, Department of Pathology and Oncology, Faculty of Medicine, University of Porto, ; 4200-319 Porto, Portugal
                [7 ]ISNI 0000 0001 1503 7226, GRID grid.5808.5, ICBAS - Instituto de Ciências Biomédicas de Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira n. 228, ; 4050-313 Porto, Portugal
                Article
                Publisher ID: 11960
                DOI: 10.1038/s41598-017-11960-0
                PMC ID: 5599645
                PubMed ID: 28912585
                SO-VID: 7843d220-ba23-4c8c-84fb-dfd6d0b1584d
                Copyright © © The Author(s) 2017
                License:

                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
                Date received : 13 January 2017
                Date accepted : 1 September 2017
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

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