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LOWER SOMATOSTATIN EXPRESSION IS AN EARLY EVENT IN DIABETIC RETINOPATHY AND IS ASSOCIATED WITH RETINAL NEURODEGENERATION

¹Diabetes Research Unit, Institut de Recerca Hospital Universitari Vall d'Hebron
²Tissue Bank and Cell Therapy Center
³Pathology, Hospital Universitari Vall d'Hebron. Universitat Autònoma de Barcelona, and
⁴Biochemistry and Molecular Biology. Universitat Autònoma de Barcelona. Barcelona, Spain

rsimo{at}ir.vhebron.net

ABSTRACT

Objective: To test hypothesis that a reduction of somatostatin (SST) in the retina exists in patients without clinically detectable diabetic retinopathy and that it is associated with retinal neurodegeneration.

Research Design and Methods: Human diabetic postmortem eyes (n=10) without clinically detectable retinopathy were compared with eyes (n=10) from non diabetic donors. SST mRNA (RT-PCR) and SST-28 immunoreactivity (confocal laser) were measured separately in neuroretina and retinal pigment epithelium (RPE). In addition, SST-28 (RIA) was measured in the vitreous fluid. Glial fibrillar acidic protein (GFAP) was assessed by immunofluorescence and Western-blot. Apoptotic cells were quantified using terminal dUTP nick-end labeling (TUNEL).

Results: A higher expression of SST was detected in RPE than in neuroretina in both groups. SST mRNA levels and SST-28 immunoreactivity were significantly lower in both RPE and the neuroretina from diabetic donors in comparison with non-diabetic donors. These results were in agreement with those obtained by measuring SST-28 in the vitreous fluid of the same donors. Increased GFAP and a higher degree of apoptosis were observed in diabetic retinas in comparison with non-diabetic retinas. These changes were most evident in those patients with the higher deficit of SST.

Conclusions: Underproduction of SST is an early event in the eyes of diabetic patients and is associated with glial activation and neural death. In addition, our results suggest that RPE is an important source of SST in the human eye. The possible role of the lower production of SST in the pathogenesis of diabetic retinopathy deserves to be investigated.

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