dermatomyositis/protease

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Autoantibodies to calpastatin (an endogenous inhibitor for calcium-dependent neutral protease, calpain) in systemic rheumatic diseases.

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We identified an autoantibody that reacts with calpastatin [an inhibitor protein of the calcium-dependent neutral protease calpain (EC 3.4.22.17)]. In early immunoblot studies, sera from patients with rheumatoid arthritis (RA) recognized unidentified 60-, 45-, and 75-kDa proteins in HeLa cell

Autoantibody against a protease domain of caspase-8 in patients with systemic sclerosis.

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BACKGROUND Systemic sclerosis (SSc) is characterized by autoantibodies against various cellular components. OBJECTIVE To determine the presence or levels of antibodies (Abs) against a protease domain (PD) of caspase-8 and their clinical relevance in SSc. METHODS Anti-caspase-8 PD Ab was examined by

Identification of granzyme B-expressing CD-8-positive T cells in lymphocytic inflammatory infiltrate in cutaneous lupus erythematosus and in dermatomyositis.

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BACKGROUND Lupus erythematosus (LE) and dermatomyositis (DM) are interface dermatitis, histologically characterized by formation of colloid bodies and a CD4+ CD8+ lymphocyte infiltrate. Colloid bodies are examples of intraepidermal apoptosis. Granzyme (Gr)B, synthesized by activated cytotoxic

The role and mechanism of cathepsin G in dermatomyositis.

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Dermatomyositis (DM) is an idiopathic inflammatory myopathy characterized by CD4+ T cells and B cells infiltration in perivascular and muscle tissue. Although the infiltration of inflammatory cells plays a key role in muscle damage, the exact mechanism is not clear. Cathepsin G (CTSG) is a member of

Cathepsins are upregulated by IFN-gamma/STAT1 in human muscle culture: a possible active factor in dermatomyositis.

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The aim of this work was to study which genes upregulated by the IFN-gamma/STAT1 system in human muscle might be involved in the process of muscle fiber atrophy in dermatomyositis (DM). These proteins included proteases (cathepsins B and L, calpain), proteins implicated in apoptosis and cell cycle

Cellular distribution of proteolytic enzymes in the skeletal muscle of sarcoid myopathy.

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To clarify the mechanism of muscle fiber destruction in sarcoid myopathy, muscle biopsy specimens were examined from patients with sarcoid myopathy, polymyositis, or dermatomyositis. In sarcoid myopathy, noncaseating granulomatous lesions were located in the perimysium or endomysium or both. Little

Granzyme B: evidence for a role in the origin of myasthenia gravis.

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OBJECTIVE Although the pathogenesis of myasthenia gravis (MG) as an antibody mediated disorder of acetylcholine receptors (AChRs) at neuromuscular junctions is well understood, the origin of the autoimmune response is unclear. The thymus is intimately involved in initiation of the autoimmune

ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease.

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The "A disintegrin and metalloprotease" (ADAM) family is thought to play an important role in tissue destruction and inflammatory reactions. ADAM-17 was first described as the protease responsible for tumor necrosis factor (TNF)-α shedding. Here, we have shown the expression of ADAM-17 in

Chemokine-like factor expression in the idiopathic inflammatory myopathies.

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OBJECTIVE We evaluated the expression of chemokine-like factor (CKLF) in biopsied muscle fibers in inflammatory myopathies, non-inflammatory myopathies and neurologically diseased controls. METHODS We studied the expression of CKLF in 15 polymyositis (PM), five dermatomyositis (DM), 15

Inducible overexpression of wild-type prion protein in the muscles leads to a primary myopathy in transgenic mice.

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The prion protein (PrP) level in muscle has been reported to be elevated in patients with inclusion-body myositis, polymyositis, dermatomyositis, and neurogenic muscle atrophy, but it is not clear whether the elevated PrP accumulation in the muscles is sufficient to cause muscle diseases. We have

How to diagnose a lipodystrophy syndrome.

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The spectrum of adipose tissue diseases ranges from obesity to lipodystrophy, and is accompanied by insulin resistance syndrome, which promotes the occurrence of type 2 diabetes, dyslipidemia and cardiovascular complications. Lipodystrophy refers to a group of rare diseases characterized by the

Calcium dysregulation, functional calpainopathy, and endoplasmic reticulum stress in sporadic inclusion body myositis.

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Sporadic inclusion body myositis (IBM) is the most common primary myopathy in the elderly, but its pathoetiology is still unclear. Perturbed myocellular calcium (Ca2+) homeostasis can exacerbate many of the factors proposed to mediate muscle degeneration in IBM, such as mitochondrial dysfunction,

Calpain inhibition attenuates intracellular changes in muscle cells in response to extracellular inflammatory stimulation.

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Idiopathic inflammatory myopathies (IIMs), comprising of polymyositis, dermatomyositis, and inclusion-body myositis, are characterized by muscle weakness and various types of inflammatory changes in muscle cells. They also show non-inflammatory changes, including perifascicular atrophy,

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