BRB_LAM_GFAP

 

NVU

 

Cldn5

 

capilary BRB

 

 

The molecular basis of the inner blood-retinal barrier

 



Breakdown of the inner endothelial blood-retinal barrier (BRB), as occurs in diabetic retinopathy, age-related macular degeneration, retinal vein occlusions, uveitis and other chronic retinal diseases, results in vasogenic edema and neural tissue damage, causing loss of vision. The central mechanism of altered BRB function is a change in the permeability characteristics of retinal endothelial cells caused by elevated levels of growth factors, cytokines, advanced glycation end products, inflammation, hyperglycemia and loss of pericytes. Subsequently, paracellular but also transcellular transport across the retinal vascular wall increases via opening of endothelial intercellular junctions and qualitative and quantitative changes in endothelial caveolar transcellular transport, respectively. Functional changes in pericytes and astrocytes, as well as structural changes in the composition of the endothelial glycocalyx and the basal lamina around BRB endothelium further facilitate BRB leakage.

The inner blood-retinal barrier (BRB) is made up by the neurovascular unit, consisting of endothelial cells, pericytes and glial cells. The BRB maintains homeostasis of the neural retina, but in pathological eye conditions the neurovascular unit is often disrupted, causing BRB loss.


Publications:

 

Expression patterns of endothelial permeability pathways in the development of the blood-retinal barrier in mice.
FASEB J (2019) 33:5320-5333.


Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological conditions. Review.
Prog Retin Eye Res (2013) 34:19-48.


Glucocorticoids exert differential effects on the endothelium in an in vitro model of the blood-retinal barrier.
cta Ophthalmol (2019) 97:214-224.


Spatial and temporal recruitment of the neurovascular unit during development of the mouse blood-retinal barrier.
Tissue and Cell (2018) 52:42-50.


TNF╬▒-Induced Disruption of the Blood-Retinal Barrier In Vitro Is Regulated by Intracellular 3',5'-Cyclic Adenosine Monophosphate Levels.
Invest Ophthalmol Vis Sci (2017) 58:3496-3505.


Plasmalemma Vesicle Associated Protein Has a Key Role in Blood-Retinal Barrier Loss.
Am J Pathol (2016) 186:1044-54.


Molecular analysis of blood-retinal barrier loss in the Akimba mouse, a model of advanced diabetic retinopathy.
Exp Eye Res (2014) 122:123-31


A novel co-culture model of the blood-retinal barrier based on primary retinal endothelial cells, pericytes and astrocytes.
Exp Eye Res (2012) 96:181-90.


Altered expression of genes related to blood-retina barrier disruption in streptozotocin-induced diabetes.
Exp Eye Res (2009) 89:4-15.