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Mechanisms of Blood–Retinal Barrier Breakdown in Diabetic Retinopathy

Ali Hafezi-Moghadam

CONTENTS

THE PROTECTIVE BARRIERS OF THE RETINA

THE INNER AND THE OUTER BRB

OTHER MEDIATORS OF LEUKOCYTE RECRUITMENT IN DR

STRUCTURAL COMPROMISE OF THE BRB

ANTI-VEGF PROPERTIES OF NATRIURETIC PEPTIDES

ACKNOWLEDGMENTS

REFERENCES

Keywords Vascular leakage • Leukocyte adhesion • ICAM-1 • b2-integrin • VAP-1

• Azurocidin (AZ) • Atrial natriuretic peptide (ANP)

The consequences of the currently growing epidemic of type 2 diabetes would soon debilitate the public health [1], unless new ways are rapidly found for prevention or therapy of the various complications of the disease.

Vascular leakage is a prominent feature of diabetic retinopathy (DR), an ocular manifestation of diabetes. Vascular leakage is routinely quantified in patients as an important end point of ocular examinations and also studied at the bench in a variety of in vitro and in vivo assays. However, despite the pertinence of vascular leakage for both research and clinic, the cellular and molecular mechanisms underlying vascular leakage are not well understood.

THE PROTECTIVE BARRIERS OF THE RETINA

A barrier function in normal blood vessels of the central nervous system (CNS) was first proposed by Paul Ehrlich (1854–1915). Reese and Karnovsky [2] later showed at an ultrastructural level that tight endothelial barriers are responsible for the unique barrier properties of CNS vessels (Fig. 1). In the eye, the blood retinal barrier (BRB) describes the selective physiological barrier that protects the neural retina from molecules and

From: Ophthalmology Research: Visual Dysfunction in Diabetes

Edited by: J. Tombran-Tink et al. (eds.), DOI 10.1007/978-1-60761-150-9_7 © Springer Science+Business Media, LLC 2012

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