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Regulation of Tight Junction Proteins in Cultured Retinal Pigment Epithelial Cells and in VEGF Overexpressing Transgenic Mouse Retinas

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Part of the book series: Advances in Experimental Medicine and Biology ((volume 572))

Abstract

Tight junctions (TJ) are specialized multiprotein complexes which act to seal the intercellular space and thereby generate a permeability barrier required for transport processes (Matter and Balda, 1999). In addition, by regulation of the TJs, the paracellular pathway may be opened for selective transport of molecules, ions (Madara et al., 1992) and neutrophils (Huber et al., 2000). Thus far several interacting constituents comprising of transmembrane proteins including occludins (OCLN-TM4+/TM4 and 1B), claudins with >20 members and a series of cytoplasmic plaque proteins including ZO-1, -2, or -3, cingulin, 7H6 and symplekin have been identified in several tissue types of different species (Citi and Cordenonsi, 1998; Furuse et al., 1993; Ghassemifar et al., 2002; Matter and Balda, 1999; Mitic and Anderson, 1998). While the inner blood-retinal barrier, the retinal vascular endothelial cells, maintain a restricted and regulated trans-/paracellular transport from the blood to the surrounding tissue, the outer blood-retinal barrier, the retinal pigment epithelium (RPE), provides a permeability barrier between the retina and the choroid allowing vectorial exchange of solutes between these layers (Thumann, 2001). The RPE plays an important role in the proper function and maintenance of the photoreceptors by releasing differentiation and survival promoting factors. Despite the identification of TJ proteins in retinal tissue, little is known about the effect of pathological insult, such as hypoxia, on the expression of TJ proteins (Mark and Davis, 2002). It has also been reported that factors present in embryonic or whole eye-extract can influence the neurons of chick sympathetic ganglia to express choline acetyltransferase (Iacovitti et al., 1987) and also support full survival ganglion neurons for up to 6 days in culture (Margiotta and Howard, 1994). Retinal hypoxia has been reported to increase production of vascular endothelial growth factor (VEGF), a known stimulant of retinal neovascularization (Okamoto et al., 1997). The aim of this study was to investigate the regulation of tight junction (TJ) gene expression in cultured retinal pigment epithelial (RPE) cells and in the retina of normal and vascular endothelial growth factor (VEGF) transgenic mice.

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Ghassemifar, R., Lai, CM., Rakoczy, P.E. (2006). Regulation of Tight Junction Proteins in Cultured Retinal Pigment Epithelial Cells and in VEGF Overexpressing Transgenic Mouse Retinas. In: Hollyfield, J.G., Anderson, R.E., LaVail, M.M. (eds) Retinal Degenerative Diseases. Advances in Experimental Medicine and Biology, vol 572. Springer, Boston, MA. https://doi.org/10.1007/0-387-32442-9_27

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  • DOI: https://doi.org/10.1007/0-387-32442-9_27

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-387-28464-4

  • Online ISBN: 978-0-387-32442-5

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