calsequestrin/воспаление

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A 63 kDa skeletal muscle protein associated with eye muscle inflammation in Graves' disease is identified as the calcium binding protein calsequestrin.

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It is generally accepted that thyroid-associated ophthalmopathy (TAO) is an autoimmune disease of the eye muscle (EM) and the surrounding orbital connective tissue in which circulating antibodies play an important role. Antibodies against EM membrane proteins of 63-67kDa mol. wt. seem to be the best

Can autoimmunity against calsequestrin explain the eye and eyelid muscle inflammation of thyroid eye disease?

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Extra-ocular and upper eyelid (levator) muscle damage in thyroid orbitopathy may be due to autoimmunity against eye muscle auto antigens. The main antigen appears to be the calcium binding protein calsequestrin. In this study we have tested for T lymphocyte sensitization to calsequestrin in patients

Peripheral blood T lymphocyte sensitisation against calsequestrin and flavoprotein in patients with Graves' ophthalmopathy.

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Thyroid-associated ophthalmopathy (TAO) is an orbital autoimmune disorder of the extraocular and eyelid muscles and surrounding connective and adipose tissue. Although mononuclear cell infiltration of orbital tissue is a characteristic feature of TAO the likely role of T lymphocyte reactivity

Changes in calsequestrin, TNF-α, TGF-β and MyoD levels during the progression of skeletal muscle dystrophy in mdx mice: a comparative analysis of the quadriceps, diaphragm and intrinsic laryngeal muscles.

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In Duchenne muscular dystrophy (DMD), the search for new biomarkers to follow the evolution of the disease is of fundamental importance in the light of the evolving gene and pharmacological therapies. In addition to the lack of dystrophin, secondary events including changes in calcium levels,

Antibodies against calsequestrin and type XIII collagen are good markers for chronic upper eyelid retraction.

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OBJECTIVE Chronic upper eyelid retraction is a common manifestation of thyroid-associated ophthalmopathy (TAO) but can occur as a dominant feature of ophthalmopathy in patients with Graves' hyperthyroidism and in association with Hashimoto's thyroiditis in the absence of other eye signs except mild

Pathogenesis of thyroid-associated ophthalmopathy: does autoimmunity against calsequestrin and collagen XIII play a role?

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Thyroid-associated ophthalmopathy (TAO), or thyroid eye disease, is a complex inflammatory disorder of the eye that, as its name implies, is associated with thyroid disease. TAO can be divided into three subtypes: ocular myopathy, congestive myopathy and mixed congestive and myopathic

Antibodies targeting the calcium binding skeletal muscle protein calsequestrin are specific markers of ophthalmopathy and sensitive indicators of ocular myopathy in patients with Graves' disease.

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We have identified several eye muscle antigens and studied the significance of the corresponding serum autoantibodies in patients with Graves' disease. Of these antigens, only calsequestrin is expressed more in eye muscle than other skeletal muscles, which could explain at least partly the specific

Extraocular muscle autoimmunity and orbital fat inflammation in thyroid-associated ophthalmopathy.

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The immunological basis for the ophthalmopathy associated with Graves' hyperthyroidism is both poorly understood and controversial. The mechanism for its link with thyroid autoimmunity is unknown but likely to be due to autoimmunity against some thyroid and orbital tissue-shared antigen, such as the

Eye muscle antibodies in patients with ocular myasthenia gravis: possible mechanism for eye muscle inflammation in acetylcholine-receptor antibody-negative patients.

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Myasthenia gravis is an organ-specific autoimmune disorder generally thought to be caused by an antibody-mediated attack against the skeletal muscle nicotinic acetylcholine (Ach) receptor (AchR) at the neuromuscular junction. Extraocular muscle weakness and double vision are present in about 90% of

Eye signs and serum eye muscle and collagen XIII antibodies in patients with transient and progressive thyroiditis.

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BACKGROUND There have been reports of the development of ophthalmopathy in patients with subacute thyroiditis (SAT) in the absence of Graves' disease and thyroid-stimulating hormone receptor (TSH-r) antibodies. OBJECTIVE The aim of the study was to determine the prevalences of eye and eyelid signs

Calreticulin, a potential vascular regulatory protein, reduces intimal hyperplasia after arterial injury.

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Both thrombotic and inflammatory responses to arterial injury have been implicated in atherosclerotic plaque growth. Calreticulin is a ubiquitous calcium-binding protein with antithrombotic activity and, in addition, is associated with leukocyte activation. We are investigating calreticulin as a

Role of eye muscle antibody measurement in diagnosis of thyroid-associated ophthalmopathy: a laboratory update.

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OBJECTIVE To review the current role of measurement of serum eye muscle antibodies in thyroid-associated ophthalmopathy (TAO). METHODS We conducted laboratory studies to determine the prevalences of serum autoantibodies reactive with eye muscle antigens in patients with active and inactive TAO,

Changes in calcium cycling precede cardiac dysfunction during autoimmune myocarditis in mice.

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Myocardial inflammation contributes to the development of dilated cardiomyopathy, as well as other cardiac diseases. We have previously shown decreased left ventricular function in mice with autoimmune myocarditis. To test the hypothesis that decreased function is mediated by changes in

Pathogenesis of thyroid eye disease--does autoimmunity against the TSH receptor explain all cases?

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Thyroid associated ophthalmopathy, or thyroid eye disease (TED), is a complex inflammatory disorder of the eye that, as its name implies, is usually associated with thyroid disease. Clinical observation supports the existence of three main TED subtypes, namely ocular myopathy, congestive myopathy,

Acute changes of biventricular gene expression in volume and right ventricular pressure overload.

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OBJECTIVE We investigated the effects of acute volume and RV pressure overload on biventricular function and gene expression of BNP, pro-inflammatory cytokines (IL-6 and TNF-alpha), iNOS, growth factors (IGF-1, ppET-1), ACE and Ca2+-handling proteins (SERCA2a, phospholamban and

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