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Alex Fonollosa, Joseba Artaraz, Agustin Martinez-Berriotxoa, Elena Vecino; Effect of Somatostatin on the expression of tight junctions and urokinase plasminogen activator receptor in human retinal pigment epithelial cells. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4511.
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© ARVO (1962-2015); The Authors (2016-present)
Somatostatin is an ubiquitous peptide with antiproliferative, antisecretory and neuroprotective properties. A role for somatostatin in the pathogenesis of macular edema has been suggested since low vitreous levels of this peptide have been found in patients with macular edema secondary to diabetic retinopathy and uveitis. However, a direct effect of somatostatin on mechanisms of regulation of blood retinal barriers has not been demonstrated. The aim of the present study was to assess the effect of somatostatin on the expression of proteins involved in this regulation: Occludin, Zonula Occludens-1 and urokinase plasminogen activator receptor, in human retinal pigment epithelial cells.
ARPE-19 cells were exposed to somatostatin under hypoxic and normoxic conditions. Immunochemistry studies for Occludin and Zonula Ocludens-1 were performed under these conditions. The mRNA expression of Occludin, Zonula Occludens-1 and urokinase plasminogen activator receptor was determined by real-time PCR, also under hypoxic and normoxic conditions. ARPE-19 cells were also exposed to vascular endothelial growth factor and to both somatostatin and vascular endothelial growth factor under normoxic conditions and the same experiments were performed.
Immunochemistry studies showed no effect of somatostatin on expression of Occludin and Zonula Occludens-1 under both hypoxic and normoxic conditions. However, mRNA expression of Ocludin, Zonula Occludens-1 and urokinase plasminogen activator receptor was increased (twofold, p<0.001, threefold, p<0.001 and threefold, p<0.001, respectively) under normoxic conditions. We did not observe any effect of vascular endothelial growth factor on tight junctions and urokinase plasminogen activator receptor expression in both immunochemistry and real-time PCR studies. Exposure to both vascular endothelial growth factor and somatostatin neither showed any effect.
Our results suggest that somatostatin may contribute to decrease permeability through the external blood retinal barrier by enhancing components of the tight junctions. Hence, a decrease in somatostatin activity may contribute to macular edema development, at least in retinal diseases in which ischaemia is not a predominant event.
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