Studies Of The Changes Of Tight Junctions And Paracellular Permeability Based On An In Vitro Inner Blood Retinal Barrier Model

Research BackgroundThe blood retinal barrier (BRB), one of the important ocular barriers, consists of two parts, inner and outer BRB. Inner BRB (iBRB) is formed by retinal microvascular endothelial cells (RMEC) and tight junctions (TJ) between them. Normal iBRB is determined by the homeostasis of retinal microvessels and plays a critical role in normal visual function. The destruction in iBRB can lead to many ocular diseases, such as diabetic macular edema which represents increased permeability of retinal microvessels, leakage from circulation, liquid aggregation in the macular zone and visual impairment.The iBRB not only shields the neural retina from external factors in the blood circulation, but also blocks the circulation pathway of medicine treatment, such as neuroprotective medicine treatments of glaucoma. Glaucoma manifests progressive vision field loss caused by damaged retinal ganglion cells as a result of elevated intraocular pressure and is one of the irreversible blind caused diseases. There is, however, no effective physical treatment for neuroprotection except filter surgery and medicine to control intraocular pressure. Nerve growth factors have been found to enhance the regeneration of neuron axiscylinder process since 1950s, but no effective neuroprotective treatment was applied in clinic because these factors could not penetrate through the iBRB to the target cells. Two methods to solve the problem are to reconstruct molecules, or to regulate the iBRB permeability. Considerable studies were focused on the first method but there was still no breakthrough. Many scientists...