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Systemic sclerosis animal model

Oliver Distler, Janet Pope, Chris Denton, Yannick Allanore, Marco Matucci-Cerinic, Janethe de Oliveira Pena, Dinesh Khanna
: RISE-SSc is a randomized, double-blind, placebo-controlled phase 2 study investigating the efficacy and safety of riociguat in patients with diffuse cutaneous systemic sclerosis (dcSSc). Based on positive results from riociguat trials in patients with pulmonary hypertension and chronic thromboembolic pulmonary hypertension in combination with the known antiproliferative and antifibrotic effects seen in animal models, patients with SSc may benefit from treatment with riociguat. Patients with SSc meeting the ACR/EULAR systemic sclerosis classification criteria with diffuse cutaneous SSc (dcSSc) subset per LeRoy criteria, and a disease duration of less than or equal to 18 months will be randomized to placebo or riociguat 0...
September 28, 2016: Respiratory Medicine
Carla Brancia, Barbara Noli, Marina Boido, Andrea Boi, Roberta Puddu, Giuseppe Borghero, Francesco Marrosu, Paolo Bongioanni, Sandro Orrù, Barbara Manconi, Filomena D'Amato, Irene Messana, Federica Vincenzoni, Alessandro Vercelli, Gian-Luca Ferri, Cristina Cocco
VGF mRNA is widely expressed in areas of the nervous system known to degenerate in Amyotrophic Lateral Sclerosis (ALS), including cerebral cortex, brainstem and spinal cord. Despite certain VGF alterations are reported in animal models, little information is available with respect to the ALS patients. We addressed VGF peptide changes in fibroblast cell cultures and in plasma obtained from ALS patients, in parallel with spinal cord and plasma samples from the G93A-SOD1 mouse model. Antisera specific for the C-terminal end of the human and mouse VGF proteins, respectively, were used in immunohistochemistry and enzyme-linked immunosorbent assay (ELISA), while gel chromatography and HPLC/ESI-MS/MS were used to identify the VGF peptides present...
2016: PloS One
Thangavelu Soundara Rajan, Domenico Scionti, Francesca Diomede, Gianpaolo Grassi, Federica Pollastro, Adriano Piattelli, Lucio Cocco, Placido Bramanti, Emanuela Mazzon, Oriana Trubiani
Research in recent years has extensively investigated the therapeutic efficacy of mesenchymal stromal cells in regenerative medicine for many neurodegenerative diseases at preclinical and clinical stages. However, the success rate of stem cell therapy remains less at translational phase. Lack of relevant animal models that potentially simulate the molecular etiology of human pathological symptoms might be a reason behind such poor clinical outcomes associated with stem cell therapy. Apparently, self-renewal and differentiation ability of mesenchymal stem cells may help to study the early developmental signaling pathways connected with the diseases, such as Alzheimer's disease, Amyotrophic lateral sclerosis (ALS), etc...
October 7, 2016: Journal of Cellular Biochemistry
Verónica Murta, Carina Ferrari
In recent decades, several neurodegenerative diseases have been shown to be exacerbated by systemic inflammatory processes. There is a wide range of literature that demonstrates a clear but complex relationship between the central nervous system (CNS) and the immunological system, both under naïve or pathological conditions. In diseased brains, peripheral inflammation can transform "primed" microglia into an "active" state, which can trigger stronger pathological responses. Demyelinating diseases are a group of neurodegenerative diseases characterized by inflammatory lesions associated with demyelination, which in turn induces axonal damage, neurodegeneration, and progressive loss of function...
2016: Advances in Experimental Medicine and Biology
Samuel S Duffy, Chamini J Perera, Preet G S Makker, Justin G Lees, Pascal Carrive, Gila Moalem-Taylor
Pain is a widespread and debilitating symptom of multiple sclerosis (MS), a chronic inflammatory demyelinating disease of the central nervous system. Although central neuroinflammation and demyelination have been implicated in MS-related pain, the contribution of peripheral and central mechanisms during different phases of the disease remains unclear. In this study, we used the animal model experimental autoimmune encephalomyelitis (EAE) to examine both stimulus-evoked and spontaneous pain behaviors, and neuroinflammatory changes, over the course of chronic disease...
2016: Frontiers in Immunology
Jason C Gardenier, Geoffrey E Hespe, Raghu P Kataru, Ira L Savetsky, Jeremy S Torrisi, Gabriela D García Nores, Joseph J Dayan, David Chang, Jamie Zampell, Inés Martínez-Corral, Sagrario Ortega, Babak J Mehrara
Development of novel treatments for lymphedema has been limited by the fact that the pathophysiology of this disease is poorly understood. It remains unknown, for example, why limb swelling resulting from surgical injury resolves initially, but recurs in some cases months or years later. Finding answers for these basic questions has been hampered by the lack of adequate animal models. In the current study, we used Cre-lox mice that expressed the human diphtheria toxin receptor (DTR) driven by a lymphatic-specific promoter in order to noninvasively ablate the lymphatic system of the hind limb...
September 22, 2016: JCI Insight
Ilona Shapira, Nina Fainstein, Maria Tsirlin, Ilana Stav, Evgenia Volinsky, Claudia Moresi, Tamir Ben-Hur, Raphael Gorodetsky
: : Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system (CNS) with no effective treatment available for the chronic-progressive stage. Cell therapy is a promising therapeutic approach for attenuating the immune-mediated CNS process. Isolated and expanded human placental stromal cells (hPSCs) possess potent immunomodulatory and trophic properties, making them a good candidate for MS therapy. We examined the potential of hPSC therapy in preventing the onset or attenuating the course of established disease in a murine MS model of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis...
September 29, 2016: Stem Cells Translational Medicine
Kirsten S Evonuk, Carson E Moseley, Ryan E Doyle, Casey T Weaver, Tara M DeSilva
A major hallmark of the autoimmune demyelinating disease multiple sclerosis (MS) is immune cell infiltration into the brain and spinal cord resulting in myelin destruction, which not only slows conduction of nerve impulses, but causes axonal injury resulting in motor and cognitive decline. Current treatments for MS focus on attenuating immune cell infiltration into the central nervous system (CNS). These treatments decrease the number of relapses, improving quality of life, but do not completely eliminate relapses so long-term disability is not improved...
2016: Journal of Visualized Experiments: JoVE
Oscar Ka-Fai Ma, Koon Ho Chan
Mesenchymal stem cells (MSCs) possess immunomodulatory properties, which confer enormous potential for clinical application. Considerable evidence revealed their efficacy on various animal models of autoimmune diseases, such as multiple sclerosis, systemic lupus erythematosus and uveitis. MSCs elicit their immunomodulatory effects by inhibiting lymphocyte activation and proliferation, forbidding the secretion of proinflammatory cytokines, limiting the function of antigen presenting cells, and inducing regulatory T (Treg) and B (Breg) cells...
September 26, 2016: World Journal of Stem Cells
Kalliopi Klavdianou, Stamatis-Nick Liossis, Lazaros Sakkas, Dimitrios Daoussis
BACKGROUND: Dickkopf-1 (Dkk-1) is a soluble inhibitor of the canonical Wnt pathway, which plays critical roles in embryonic development. Evidence suggests that this molecule regulates several aspects of both bone biology and fibrosis. OBJECTIVES: To provide an overview of our current knowledge of the role of Dkk-1 in joint remodeling and fibrosis. METHODS: We performed an electronic search (Medline) using the following key words: Dickkopf-1 (or Dkk-1), new bone formation, joint remodeling, ankylosing spondylitis, systemic sclerosis (or scleroderma), and fibrosis, supplemented by a manual search of references from retrieved articles...
August 23, 2016: Seminars in Arthritis and Rheumatism
T Draheim, A Liessem, M Scheld, F Wilms, M Weißflog, B Denecke, T W Kensler, A Zendedel, C Beyer, M Kipp, C J Wruck, A Fragoulis, T Clarner
Oxidative stress critically contributes to the pathogenesis of a variety of neurodegenerative diseases such as multiple sclerosis. Astrocytes are the main regulators of oxidative homeostasis in the brain and dysregulation of these cells likely contributes to the accumulation of oxidative damage. The nuclear factor erythroid 2-related factor 2 (Nrf2) is the main transcriptional regulator of the anti-oxidant stress defense. In this study, we elucidate the effects of astrocytic Nrf2-activation on brain-intrinsic inflammation and lesion development...
September 19, 2016: Glia
So Jin Bing, Danbee Ha, Insun Hwang, Eunjin Park, Ginnae Ahn, Jie-Young Song, Youngheun Jee
Bearing pathologic and clinical similarities to human multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE) is used as a murine model to test potential therapeutic agents for MS. Recently, we reported the protective effects of an acidic polysaccharide of Panax ginseng (APG) in C57BL/6 strain-dependent EAE, a model of primary progressive MS. In this study, we extend our previous findings on the therapeutic capacity of APG in relapsing-remitting EAE (rr-EAE), the animal model to closely mimic recurrent inflammatory demyelination lesions of relapsing-remitting MS...
2016: American Journal of Chinese Medicine
Lazaros I Sakkas
Systemic sclerosis (SSc) is a multisystem disease characterized by extensive collagen deposition in skin and internal organs, fibrointimal microvasculopathy, and activation of the immune system. T cells and B cells can promote fibrosis in SSc. Interleukin (IL)-6 is implicated in the pathogenesis of SSc. IL-6 is increased in the peripheral blood and lesional skin from patients with SSc, and induces fibroblast collagen production directly and indirectly by inducing profibrotic M2 macrophages. IL-6 also induces Th17 differentiation and promotes B cell differentiation toward Ig-producing plasma cells...
2016: Drug Design, Development and Therapy
Michal Schwartz, Aleksandra Deczkowska
Neuroinflammation is common to various diseases of the central nervous system (CNS), but its imprecise definition has led to many misconceptions in research and clinical approaches. It is now recognized that neuroinflammation in chronic neurodegenerative conditions, including Alzheimer's disease (AD) and age-related dementia, is distinct from the inflammation that accompanies relapsing-remitting multiple sclerosis (RRMS), and its experimental animal model, experimental autoimmune encephalomyelitis (EAE). Here, we discuss the discrete features of inflammation in different CNS pathologies, given the current understanding of the CNS-immune crosstalk; the roles of the immune cells that are involved, their phenotypes, and their location and route of entry to the CNS...
October 2016: Trends in Immunology
Ann-Kathrin Uhde, Vanessa Herder, Muhammad Akram Khan, Malgorzata Ciurkiewicz, Dirk Schaudien, René Teich, Stefan Floess, Wolfgang Baumgärtner, Jochen Huehn, Andreas Beineke
Theiler´s murine encephalomyelitis virus (TMEV)-infection is a widely used animal model for studying demyelinating disorders, including multiple sclerosis (MS). The immunosuppressive cytokine Interleukin (IL)-10 counteracts hyperactive immune responses and critically controls immune homeostasis in infectious and autoimmune disorders. In order to investigate the effect of signaling via Interleukin-10 receptor (IL-10R) in infectious neurological diseases, TMEV-infected SJL mice were treated with IL-10R blocking antibody (Ab) in the acute and chronic phase of the disease...
2016: PloS One
Manuela Cerina, Venu Narayanan, Kerstin Göbel, Stefan Bittner, Tobias Ruck, Patrick Meuth, Alexander M Herrmann, Martin Stangel, Viktoria Gudi, Thomas Skripuletz, Thiemo Daldrup, Heinz Wiendl, Thomas Seidenbecher, Petra Ehling, Christoph Kleinschnitz, Hans-Christian Pape, Thomas Budde, Sven G Meuth
Myelin loss is a severe pathological hallmark common to a number of neurodegenerative diseases, including multiple sclerosis (MS). Demyelination in the central nervous system appears in the form of lesions affecting both white and gray matter structures. The functional consequences of demyelination on neuronal network and brain function are not well understood. Current therapeutic strategies for ameliorating the course of such diseases usually focus on promoting remyelination, but the effectiveness of these approaches strongly depends on the timing in relation to the disease state...
August 25, 2016: Brain, Behavior, and Immunity
Roberta G Marangoni, John Varga, Warren G Tourtellotte
PURPOSE OF REVIEW: We discuss recent advances in evaluating and optimizing animal models of systemic sclerosis (SSc). Such models could be of value for illuminating etiopathogenesis using hypothesis-testing experimental approaches, for developing effective disease-modifying therapies, and for uncovering clinically relevant biomarkers. RECENT FINDINGS: We describe recent advances in previously reported and novel animal models of SSc. The limitations of each animal model and their ability to recapitulate the pathophysiology of recognized molecular subsets of SSc are discussed...
November 2016: Current Opinion in Rheumatology
Lorelei Stoica, Miguel Sena-Esteves
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease caused by progressive loss of upper and lower motor neurons. Mutations in superoxide dismutase 1 (SOD1) are a leading cause of ALS, responsible for up to 20% of familial cases. Although the exact mechanism by which mutant SOD1 causes disease remains unknown, multiple studies have shown that reduction of the mutant species leads to delayed disease onset and extension of lifespan of animal models. This makes SOD1 an ideal target for gene therapy coupling adeno associated virus vector (AAV) gene delivery with RNAi molecules...
2016: Frontiers in Molecular Neuroscience
Martin M Herrmann, Silvia Barth, Bernhard Greve, Kathrin M Schumann, Andrea Bartels, Robert Weissert
After encounter with a central nervous system (CNS)-derived autoantigen, lymphocytes leave the lymph nodes and enter the CNS. This event leads only rarely to subsequent tissue damage. Genes relevant to CNS pathology after cell infiltration are largely undefined. Myelin-oligodendrocyte-glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), a chronic autoimmune disease of the CNS that results in disability. To assess genes that are involved in encephalitogenicity and subsequent tissue damage mediated by CNS-infiltrating cells, we performed a DNA microarray analysis from cells derived from lymph nodes and eluted from CNS in LEW...
October 1, 2016: Disease Models & Mechanisms
Kai Zhang, Yawei Guo, Zhenzhen Ge, Zhihui Zhang, Yurong Da, Wen Li, Zimu Zhang, Zhenyi Xue, Yan Li, Yinghui Ren, Long Jia, Koon-Ho Chan, Fengrui Yang, Jun Yan, Zhi Yao, Aimin Xu, Rongxin Zhang
T helper 17 (Th17) cells are vital components of the adaptive immune system involved in the pathogenesis of most autoimmune and inflammatory syndromes, and adiponectin(ADN) is correlated with inflammatory diseases such as multiple sclerosis (MS) and type II diabetes. However, the regulatory effects of adiponectin on pathogenic Th17 cell and Th17-mediated autoimmune central nervous system (CNS) inflammation are not fully understood. In this study, we demonstrated that ADN could inhibit Th1 and Th17 but not Th2 cells differentiation in vitro...
August 11, 2016: Molecular Neurobiology
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