TSH receptor protein is selectively expressed in normal human extraocular muscle

Kloprogge, S J; Busuttil, Bridget E.; Frauman, Albert G

doi:10.1002/mus.20315

Cited by 16 publications

(7 citation statements)

References 12 publications

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“…However, TSH-R was expressed in a similar amount compared to the expression level in mouse hypothalamic tissue, where TSH-R is reported to be present [12]. Also, we confirmed that the PCR bands were the true TSH-R using a direct sequencing method after DNA extraction from the expected bands.…”

Section: Discussionsupporting

confidence: 75%

Expression of Thyroid Stimulating Hormone Receptor mRNA in Mouse C2C12 Skeletal Muscle Cells

et al. 2013

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BackgroundWe analyzed whether thyroid stimulating hormone receptor (TSH-R) is expressed in a skeletal muscle cell line and if TSH has influence on the differentiation of muscle cells or on the determination of muscle fiber types.MethodsTSH-R gene expression was detected with nested real-time polymerase chain reaction (RT-PCR) in C2C12, a mouse skeletal muscle cell line. The effect of TSH on myotube differentiation was assessed by microscopic examination of myotube formation and through the measurement of expression of muscle differentiation markers, i.e., myogenin and myoD, and muscle type-specific genes, i.e., MyHC1, MyHC2a, and MyHC2b, with quantitative RT-PCR before and after incubation of C2C12 myotube with TSH.ResultsTSH-R was expressed in the mouse skeletal muscle cell line. However, treatment with TSH had little effect on the differentiation of muscle cells, although the expression of the muscle differention marker myogenin was significantly increased after TSH treatment. Treatment of TSH did not affect the expression of muscle type-specific genes.ConclusionTSH-R is expressed in a mouse skeletal muscle cell line, but the role of TSH receptor signaling in skeletal muscle needs further investigation.

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Section: Discussionsupporting

confidence: 75%

Expression of Thyroid Stimulating Hormone Receptor mRNA in Mouse C2C12 Skeletal Muscle Cells

et al. 2013

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“…A remaining central question concerns the identity of the primary autoimmune target in TAO. Extraocular muscle has been proposed by a few investigators, [92][93][94][95][96][97] but most have focused on orbital fibroblasts. 98 Supporting the latter point of view, infiltrating CD8 þ T cells recognize orbital fibroblasts, and become activated through MHC class II and CD40-dependent signaling, 7 suggesting that these cells represent autoimmune targets.…”

Section: Orbital Fibroblasts and The Putative Role Of Bone Marrow-dermentioning

confidence: 99%

Current Concepts in the Molecular Pathogenesis of Thyroid-Associated Ophthalmopathy

Wang¹,

Smith²

2014

Invest. Ophthalmol. Vis. Sci.

195

156

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Graves' disease (GD) is a common autoimmune condition. At its core, stimulatory autoantibodies are directed at the thyroid-stimulating hormone receptor (TSHR), resulting in dysregulated thyroid gland activity and growth. Closely associated with GD is the ocular condition known as thyroid-associated ophthalmopathy (TAO). The pathogenesis of TAO remains enigmatic as do the connections between the thyroid and orbit. This review highlights the putative molecular mechanisms involved in TAO and suggests how these insights provide future directions for identifying therapeutic targets. Genetic, epigenetic, and environmental factors have been suggested as contributory to the development of GD and TAO. Thyroid-stimulating hormone receptor and insulin-like growth factor receptor (IGF-1R) are expressed at higher levels in the orbital connective tissue from individuals with TAO than in healthy tissues. Together, they form a functional complex and appear to promote signaling relevant to GD and TAO. Orbital fibroblasts display an array of cell surface receptors and generate a host of inflammatory molecules that may participate in T and B cell infiltration. Recently, a population of orbital fibroblasts has been putatively traced to bone marrow-derived progenitor cells, known as fibrocytes, as they express CD45, CD34, CXCR4, collagen I, functional TSHR, and thyroglobulin (Tg). Fibrocytes become more numerous in GD and we believe traffic to the orbit in TAO. Numerous attempts at developing complete animal models of GD have been largely unsuccessful, because they lack fidelity with the ocular manifestations seen in TAO. Better understanding of the pathogenesis of TAO and development of improved animal models should greatly accelerate the identification of medical therapy for this vexing medical problem.

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“…In general, the evidence for TSHR in extraocular muscle is less abundant than the data demonstrating TSHR in adipose tissue. The selective expression of TSHR in extraocular muscle reported by Kloprogge et al (2005) contrasts with the more widespread nature of TSHR expression in various GD fat depots . The extraocular muscle enlargement in GO has previously been considered to be the result of inflammation and oedema rather than hyperplasia or hypertrophy of the myocytes themselves (Hufnagel et al 1987).…”

Section: Tshr and Musclementioning

confidence: 75%

TSH receptor activation and body composition

Lloyd

Bursell²,

Gregory³

et al. 2009

Journal of Endocrinology

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The impacts of hyper and hypothyroidism on body composition, i.e. the relative quantity and quality of bone, adipose tissue and muscle, have traditionally been attributed uniquely to abnormal levels of free thyroid hormones. The presence of biologically active TSH receptors in bone, fat and muscle, raises the possibility that both thyroid hormones and TSH contribute to the changes in body composition associated with thyroid disease. This review evaluates the evidence for this in terms of the in vitro experimental approaches applied, data from in vivo sources (i.e. mouse models) and patient-based studies.

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TSH receptor protein is selectively expressed in normal human extraocular muscle

Cited by 16 publications

References 12 publications

Expression of Thyroid Stimulating Hormone Receptor mRNA in Mouse C2C12 Skeletal Muscle Cells

Expression of Thyroid Stimulating Hormone Receptor mRNA in Mouse C2C12 Skeletal Muscle Cells

Current Concepts in the Molecular Pathogenesis of Thyroid-Associated Ophthalmopathy

TSH receptor activation and body composition

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