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      Animal models of systemic sclerosis: their utility and limitations

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          Abstract

          Without doubt, animal models have provided significant insights into our understanding of the rheumatological diseases; however, no model has accurately replicated all aspects of any autoimmune disease. Recent years have seen a plethora of knockouts and transgenics that have contributed to our knowledge of the initiating events of systemic sclerosis, an autoimmune disease. In this review, the focus is on models of systemic sclerosis and how they have progressed our understanding of fibrosis and vasculopathy, and whether they are relevant to the pathogenesis of systemic sclerosis.

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          Caveolae: from cell biology to animal physiology.

          Babak Razani, Scott E Woodman, Michael Lisanti (2002)
          Among the membrane compartments of a cell, vesicles known as "caveolae" have long defied functional characterization. However, since the identification of a family of proteins termed "caveolins", that form and reside in caveolae, a better understanding has emerged. It is now clear that caveolae do not merely play a singular role in the cell, but are pleiotropic in nature-serving to modulate many cellular functions. The purpose of this review is to explicate what is known about caveolins/caveolae and highlight growing areas of caveolar research.
          Article 0 comments Cited 176 times – based on 0 reviews     Review now
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            IL-1R1/MyD88 signaling and the inflammasome are essential in pulmonary inflammation and fibrosis in mice.

            Paméla Gasse, Caroline Mary, Isabelle Guenon … (2007)
            The molecular mechanisms of acute lung injury resulting in inflammation and fibrosis are not well established. Here we investigate the roles of the IL-1 receptor 1 (IL-1R1) and the common adaptor for Toll/IL-1R signal transduction, MyD88, in this process using a murine model of acute pulmonary injury. Bleomycin insult results in expression of neutrophil and lymphocyte chemotactic factors, chronic inflammation, remodeling, and fibrosis. We demonstrate that these end points were attenuated in the lungs of IL-1R1- and MyD88-deficient mice. Further, in bone marrow chimera experiments, bleomycin-induced inflammation required primarily MyD88 signaling from radioresistant resident cells. Exogenous rIL-1beta recapitulated a high degree of bleomycin-induced lung pathology, and specific blockade of IL-1R1 by IL-1 receptor antagonist dramatically reduced bleomycin-induced inflammation. Finally, we found that lung IL-1beta production and inflammation in response to bleomycin required ASC, an inflammasome adaptor molecule. In conclusion, bleomycin-induced lung pathology required the inflammasome and IL-1R1/MyD88 signaling, and IL-1 represented a critical effector of pathology and therapeutic target of chronic lung inflammation and fibrosis.
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              An Involvement of Oxidative Stress in Endoplasmic Reticulum Stress and Its Associated Diseases

              Bidur Bhandary, Anu Marahatta, Hyung-Ryong Kim … (2012)
              The endoplasmic reticulum (ER) is the major site of calcium storage and protein folding. It has a unique oxidizing-folding environment due to the predominant disulfide bond formation during the process of protein folding. Alterations in the oxidative environment of the ER and also intra-ER Ca2+ cause the production of ER stress-induced reactive oxygen species (ROS). Protein disulfide isomerases, endoplasmic reticulum oxidoreductin-1, reduced glutathione and mitochondrial electron transport chain proteins also play crucial roles in ER stress-induced production of ROS. In this article, we discuss ER stress-associated ROS and related diseases, and the current understanding of the signaling transduction involved in ER stress.
              Article 0 comments Cited 132 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Open Access Rheumatol
                Journal ID (iso-abbrev): Open Access Rheumatol
                Journal ID (publisher-id): Open Access Rheumatology: Research and Reviews
                Title: Open Access Rheumatology : Research and Reviews
                Publisher: Dove Medical Press
                ISSN (Electronic): 1179-156X
                Publication date Collection: 2014
                Publication date (Electronic): 01 July 2014
                Volume: 6
                Pages: 65-81
                Affiliations
                Department of Microbiology and Immunology, Drexel University College of Medicine, Philadelphia, PA, USA
                Author notes
                Correspondence: Carol M Artlett, Department of Microbiology and Immunology, Drexel University College of Medicine, 2900 Queen Lane, Philadelphia, PA 19129, USA, Tel +1 215 991 8585, Fax +1 215 848 2271, Email carol.artlett@ 123456drexelmed.edu
                Article
                Publisher ID: oarrr-6-065
                DOI: 10.2147/OARRR.S50009
                PMC ID: 5045111
                PubMed ID: 27790036
                SO-VID: 9aa7166a-d75f-406d-8226-2971bb9fc304
                Copyright © © 2014 Artlett. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License
                License:

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Subject: Review

                Keywords: systemic sclerosis,animal models,vasculopathy,fibrosis,chicken,mouse
                Data availability:
                Keywords: systemic sclerosis, animal models, vasculopathy, fibrosis, chicken, mouse

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