Expression of thyrotropin-receptor mRNA in healthy and Graves' disease retro-orbital tissue

Feliciello, Antonio; Porcellini, Antonio; Ciullo, Ilaria; Bonavolontà, Giulio; Avvedimento, E V; Fenzi, Gianfranco

doi:10.1016/0140-6736(93)91475-2

Cited by 279 publications

(130 citation statements)

References 7 publications

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“…This work confirmed earlier PCR based studies, which had indicated increased TSHR expression in orbital fat (Feliciello et al 1993) from patients with Graves' ophthalmopathy (GO). In this orbital condition, there is expansion of the orbital contents which results in proptosis (Ludgate & Baker 2002).…”

Section: Tshr and Adipose Tissuesupporting

confidence: 80%

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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Section: Tshr and Adipose Tissuesupporting

confidence: 80%

TSH receptor activation and body composition

Lloyd

Bursell²,

Gregory³

et al. 2009

Journal of Endocrinology

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“…Results of these studies were in general agreement and demonstrated the presence of TSHR mRNA and protein in orbital adipose tissue specimens and derivative cultures from patients with GO and from patients without GO. [13][14][15] However, additional studies showed that levels of TSHR are in fact higher in orbital adipose tissue from patients with GO than from patients without GO, suggesting that increased TSHR expression in the orbit might be involved in disease development. 16 This concept is further supported by the finding of a positive correlation between GO patients' TSHR mRNA levels in orbital adipose tissues excised during decompression surgery and the patients' clinical activity score.…”

mentioning

confidence: 99%

Pathogenesis of Graves Ophthalmopathy: Implications for Prediction, Prevention, and Treatment

Garrity

Bahn

2006

American Journal of Ophthalmology

213

151

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PURPOSE-To review current concepts regarding the pathogenesis of Graves ophthalmopathy (GO). We have presented this information in the context of potential target sites for novel disease therapies. DESIGN-Review of recent literature. METHODS-Synthesis of recent literature.RESULTS-Enlargement of the extraocular muscle bodies and expansion of the orbital fatty connective tissues is apparent in patients with GO. These changes result from abnormal hyaluronic acid accumulation and edema within these tissues and expanded volume of the orbital adipose tissues. Recent studies have suggested that the increase in orbital fat volume is caused by stimulation of adipogenesis within these tissues. The orbital fibroblast appears to be the major target cell of the autoimmune process in GO. A subset of these cells is capable of producing hyaluronic acid and differentiating into mature adipocytes, given appropriate stimulation. In addition, orbital fibroblasts from patients with GO have been shown to display immunoregulatory molecules and to express both thyrotropin receptors (TSHRs) and insulin-like growth factor 1 receptors (IGF-1Rs). Increased TSHR expression in the GO orbit appears to be the result of stimulated adipocyte differentiation. The activation of IGF-1R on orbital fibroblasts by immunoglobulins from GO patients results in increased production of both hyaluronic acid and molecules that stimulate the infiltration of activated T cells into areas of inflammation.

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“…Thyroid-stimulating antibodies directed against the TSH receptor could interact with the orbital components that express the receptor, thus stimulating glycosaminoglycans, cellular matrix proteins and connective tissue production and bringing about antibodydependent cell-mediated cytotoxicity mediated by natural killer cells. On the other hand, T cells that react with the TSH receptor will be targeted to the orbit where, in the presence of the antigen, they will secrete various cytokines that stimulate fibroblasts to proliferate, to express the major complex of histocompatibility class II antigens and to synthesize collagen and connective tissue (10).…”

Section: Introductionmentioning

confidence: 99%