Abstract
The outer blood retina barrier (oBRB) formed by the retinal pigment epithelium (RPE) is critical for maintaining retinal homeostasis. Critical to this modified neuro-epithelial barrier is the presence of the tight junction structure that is formed at the apical periphery of contacting cells. This tight junction complex mediates size-selective passive diffusion of solutes to and from the outer segments of the retina. Unlike other epithelial cells, the apical surface of the RPE is in direct contact with neural tissue and it is centrally involved in the daily phagocytosis of the effete tips of photoreceptor cells. While much is known about the intracellular trafficking of material within the RPE, less is known about the role of the tight junction complexes in health and diseased states. Here, we provide a succinct overview of the molecular composition of the RPE tight junction complex in addition to highlighting some of the most common retinopathies that involve a dysregulation of RPE integrity
Highlights
The blood retina barrier (BRB) is fundamental in establishing and maintaining a suitable environment for optimum retinal function [1]
We will discuss how the disruption of the outer blood retina barrier (oBRB) contributes to the pathogenesis of a range of ocular pathologies namely diabetic retinopathy (DR), and diabetic macular oedema (DMO), age related macular degeneration (AMD), central serous chorioretinopathy (CSCR), Sorsby’s fundal dystrophy, and Retinitis Pigmentosa (RP), and examine conditions associated with mutations in CLDN-19
It is the integrity of the oBRB that keeps the choroidal vascular response from invading the retina and changing dry into wet AMD [1] and the loss of this retinal pigment epithelium (RPE)–RPE attachment can induce Vascular endothelial growth factor (VEGF) overexpression [60]
Summary
The blood retina barrier (BRB) is fundamental in establishing and maintaining a suitable environment for optimum retinal function [1]. The TJs create a barrier to paracellular diffusion of solutes as well as the maintenance of cell polarity between the basolateral and apical plasma membrane domains, which are often referred to as the “barrier” and “fence” function, respectively [17]. Since their identification via electron microscopy in 1963, we have learnt a great deal more about the location and composition of TJs [18]. This displays the role of ZO-1 in a wide portfolio of cellular functions in addition to mediating barrier function [3]
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