HMGB1 and RAGE in skeletal muscle inflammation: Implications for protein accumulation in inclusion body myositis

[1]  V. Limaye,et al.  Major Histocompatibility Complex Class I and II Expression in Idiopathic Inflammatory Myopathy , 2013, Applied immunohistochemistry & molecular morphology : AIMM.

[2]  M. Dalakas,et al.  Inclusion body myositis: from immunopathology and degenerative mechanisms to treatment perspectives , 2013, Expert review of clinical immunology.

[3]  J. Lünemann,et al.  TNF-α upregulates macroautophagic processing of APP/β-amyloid in a human rhabdomyosarcoma cell line , 2013, Journal of the Neurological Sciences.

[4]  H. Westerblad,et al.  TLR4 as receptor for HMGB1 induced muscle dysfunction in myositis , 2012, Annals of the rheumatic diseases.

[5]  W. Engel,et al.  Pathogenic Considerations in Sporadic Inclusion-Body Myositis, a Degenerative Muscle Disease Associated With Aging and Abnormalities of Myoproteostasis , 2012, Journal of neuropathology and experimental neurology.

[6]  J. Pei,et al.  AGEs Induce Cell Death via Oxidative and Endoplasmic Reticulum Stresses in Both Human SH-SY5Y Neuroblastoma Cells and Rat Cortical Neurons , 2012, Cellular and Molecular Neurobiology.

[7]  R. Gold,et al.  Nitric oxide stress in sporadic inclusion body myositis muscle fibres: inhibition of inducible nitric oxide synthase prevents interleukin-1β-induced accumulation of β-amyloid and cell death. , 2012, Brain : a journal of neurology.

[8]  U. Andersson,et al.  HMGB1: A multifunctional alarmin driving autoimmune and inflammatory disease , 2012, Nature Reviews Rheumatology.

[9]  Minhyung Lee,et al.  Extracellular HMGB1 Released by NMDA Treatment Confers Neuronal Apoptosis via RAGE-p38 MAPK/ERK Signaling Pathway , 2011, Neurotoxicity Research.

[10]  H. Westerblad,et al.  Effects of HMGB1 on in vitro responses of isolated muscle fibers and functional aspects in skeletal muscles of idiopathic inflammatory myopathies , 2010, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[11]  Ho‐Youn Kim,et al.  Expression of TLR2, TLR4, and TLR9 in dermatomyositis and polymyositis , 2009, Clinical Rheumatology.

[12]  B. De Paepe,et al.  Role of cytokines and chemokines in idiopathic inflammatory myopathies , 2009, Current opinion in rheumatology.

[13]  Stephan Saalfeld,et al.  Globally optimal stitching of tiled 3D microscopic image acquisitions , 2009, Bioinform..

[14]  M. Dalakas,et al.  Interrelation of inflammation and APP in sIBM: IL-1β induces accumulation of β-amyloid in skeletal muscle , 2008, Brain : a journal of neurology.

[15]  S. Houser,et al.  Negative inotropic effects of high-mobility group box 1 protein in isolated contracting cardiac myocytes. , 2008, American journal of physiology. Heart and circulatory physiology.

[16]  E. Abraham,et al.  HMGB1 Develops Enhanced Proinflammatory Activity by Binding to Cytokines1 , 2008, The Journal of Immunology.

[17]  M. Haslbeck,et al.  Factors masking HMGB1 in human serum and plasma , 2007, Journal of leukocyte biology.

[18]  K. Tracey,et al.  High mobility group box‐1 protein induces the migration and activation of human dendritic cells and acts as an alarmin , 2007, Journal of leukocyte biology.

[19]  A. Maseri,et al.  Smooth muscle cells in human atherosclerotic plaques secrete and proliferate in response to high mobility group box 1 protein , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[20]  M. Dalakas,et al.  Sporadic inclusion body myositis—diagnosis, pathogenesis and therapeutic strategies , 2006, Nature Clinical Practice Neurology.

[21]  H. Wiendl,et al.  Expression of toll‐like receptors by human muscle cells in vitro and in vivo: TLR3 is highly expressed in inflammatory and HIV myopathies, mediates IL‐8 release, and up‐regulation of NKG2D‐ligands , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[22]  E. Schleicher,et al.  The RAGE pathway in inflammatory myopathies and limb girdle muscular dystrophy , 2005, Acta Neuropathologica.

[23]  E. Hoffman,et al.  Activation of the endoplasmic reticulum stress response in autoimmune myositis: potential role in muscle fiber damage and dysfunction. , 2005, Arthritis and rheumatism.

[24]  M. Dalakas,et al.  Upregulated inducible co-stimulator (ICOS) and ICOS-ligand in inclusion body myositis muscle: significance for CD8+ T cell cytotoxicity. , 2004, Brain : a journal of neurology.

[25]  U. Andersson,et al.  Down-regulation of the aberrant expression of the inflammation mediator high mobility group box chromosomal protein 1 in muscle tissue of patients with polymyositis and dermatomyositis treated with corticosteroids. , 2004, Arthritis and rheumatism.

[26]  K. Tracey,et al.  Reversing established sepsis with antagonists of endogenous high-mobility group box 1 , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[27]  R. Hohlfeld,et al.  Polymyositis and dermatomyositis , 2003, The Lancet.

[28]  M. Dalakas,et al.  Expression of IFN-γ-inducible chemokines in inclusion body myositis , 2003, Journal of Neuroimmunology.

[29]  H. Harris,et al.  Successful treatment of collagen-induced arthritis in mice and rats by targeting extracellular high mobility group box chromosomal protein 1 activity. , 2003, Arthritis and rheumatism.

[30]  M. Bianchi,et al.  The nuclear protein HMGB1 is secreted by monocytes via a non‐classical, vesicle‐mediated secretory pathway , 2002, EMBO reports.

[31]  T. Misteli,et al.  Release of chromatin protein HMGB1 by necrotic cells triggers inflammation , 2002, Nature.

[32]  G. Schuler,et al.  Induction of iNOS expression in skeletal muscle by IL-1β and NFκB activation: an in vitro and in vivo study , 2002 .

[33]  K. Tracey,et al.  High Mobility Group 1 Protein (Hmg-1) Stimulates Proinflammatory Cytokine Synthesis in Human Monocytes , 2000, The Journal of experimental medicine.

[34]  W. Engel,et al.  Association of active extracellular signal-regulated protein kinase with paired helical filaments of inclusion-body myositis muscle suggests its role in inclusion-body myositis tau phosphorylation. , 2000, The American journal of pathology.

[35]  Nagaraju,et al.  A variety of cytokines and immunologically relevant surface molecules are expressed by normal human skeletal muscle cells under proinflammatory stimuli , 1998, Clinical and experimental immunology.

[36]  W. Tourtellotte,et al.  Amyloid-beta peptide-receptor for advanced glycation endproduct interaction elicits neuronal expression of macrophage-colony stimulating factor: a proinflammatory pathway in Alzheimer disease. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[37]  J. Chen,et al.  The Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin , 1995, The Journal of Biological Chemistry.

[38]  Heng Du,et al.  RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer's disease. , 2012, Frontiers in bioscience.

[39]  G. Borm,et al.  Diagnostic value of MHC class I staining in idiopathic inflammatory myopathies. , 2004, Journal of neurology, neurosurgery, and psychiatry.

[40]  Hong Wang,et al.  Structural Basis for the Proinflammatory Cytokine Activity of High Mobility Group Box 1 , 2003, Molecular medicine.