Publications by authors named "Fiona Grennan-Jones"

Thyroid stimulating antibodies (TSAB) cause Graves' disease and contribute to Graves' Orbitopathy (GO) pathogenesis. We hypothesise that the presence of TSH binding proteins (truncated variants ()) and/or nonclassical ligands such as () might provide a mechanism to protect against or exacerbate GO. We analysed primary orbital preadipocyte-fibroblasts (OF) from GO patients and people free of GO (non-GO).

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Background: In Graves' orbitopathy (GO), increased proliferation, excess adipogenesis, and hyaluronan overproduction produce GO exophthalmos. Enophthalmos occurs in some glaucoma patients treated with Bimatoprost (prostaglandin F2α, PGF2α) eye drops. We hypothesized that enophthalmos is secondary to reductions in orbital tissue proliferation, adipogenesis, and/or increased lipolysis.

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Context: Graves' orbitopathy (GO) is associated with Graves' disease, in which anti-TSH receptor (TSHR) autoantibodies (thyroid-stimulating antibodies) increase cAMP causing hyperthyroidism. Excess adipogenesis and hyaluronan (HA) overproduction [HA synthase 2 (HAS2) is the major source] expand the orbital contents causing GO. TSHR activation participates in both processes but an anti-TSHR monoclonal without TSAB activity also increased HA, suggesting the involvement of other cascades.

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The thyrotropin receptor (TSHR) is expressed during lineage-specific differentiation (e.g. adipogenesis) and is activated by TSH, thyroid-stimulating antibodies, and gain-of-function mutations (TSHR*).

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Since TSH receptor (TSHR) expression increases during adipogenesis and signals via cAMP/phospho-cAMP-response element binding protein (CREB), reported to be necessary and sufficient for adipogenesis, we hypothesised that TSHR activation would induce preadipocyte differentiation. Retroviral vectors introduced constitutively active TSHR (TSHR*) into 3T3L1 preadipocytes; despite increased cAMP (RIA) and phospho-CREB (western blot) there was no spontaneous adipogenesis (assessed morphologically, using oil red O and QPCR measurement of adipogenesis markers). We speculated that Gbetagamma signalling may be inhibitory but failed to induce adipogenesis using activated Gsalpha (gsp*).

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