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Submitted on November 19, 2004
Accepted on May 20, 2005
Department of Endocrinology, Wallenberg Laboratory, Department of Ophthalmology and 3 Department of Plastic Surgery, Malmö University Hospital, S-205 02 Malmö, Sweden
* To whom correspondence should be addressed. E-mail: Mikael.Lantz{at}endo.mas.lu.se.
Context: In Graves' ophthalmopathy a major problem is an increase in the intraorbital adipose tissue volume.
Objective: The aim of this work was to define mechanisms of orbital adipogenesis.
Design: Open-label prospective.
Setting: Clinic of Endocrinology, University Hospital.
Participants: Patients (n = 5) with severe ophthalmopathy with affection of the optic nerve and thyroid healthy controls (n = 5).
Interventions: Lateral decompression of orbital tissue in patients unresponsive to corticosteroids and restorative surgery of the upper eyelid in thyroid healthy controls.
Main Outcome Measure: Large scale measurement of gene expression, with microarray technique, based on determination of fluorescence intensities in cases and controls.
Results: A marker of adipose tissue, SCD, was overexpressed in ophthalmopathy and selection criteria were set to favor identification of genes known to be expressed in normal adipogenesis. The immediate early gene CYR61 was overexpressed in addition to 15 other IEGs and the expressions of selected IEGs was confirmed with RT-PCR; CYR61, COX-2, DUSP1, BTG2 and EGR1. CYR61-responsive genes, known to participate in inflammation, IL-1beta, MMP-3 and VEGF were also overexpressed. Patients showed greater expression of CYR61 in the active than the chronic phase of ophthalmopathy, indicating that CYR61 is a marker of disease activity. COX-2 the target gene of IL-1beta, was also overexpressed although all patients had been treated with corticosteroids.
Conclusion: Adipocyte related IEGs are overexpressed in active ophthalmopathy and CYR61 may have a role in both orbital inflammation and adipogenesis and serve as a marker of disease activity.
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