Changes in ocular aquaporin expression following optic nerve crush.

Purpose: Changes in the expression of water channels (aquaporins; AQP) have been reported in several diseases. However, such changes and mechanisms remain to be evaluated for retinal injury after optic nerve crush (ONC). This study was designed to analyze changes in the expression of AQP4 (water selective channel) and AQP9 (water and lactate channel) following ONC in the rat.

Involvement of P2X7 receptors in the hypoxia-induced death of rat retinal neurons.

Purpose: To investigate the hypoxia-induced death of rat retinal neurons and to determine whether P2X(7) activation is involved in this type of neuronal death.

Methods: Cultured retinal neurons from fetal rats were used. The effects and time course of various degrees of hypoxia (1%-5% O(2)) in the death of retinal neurons, were examined.

Endothelin-1 (ET-1) is increased in rat retina after crushing optic nerve.

Purpose: To determine the alterations in the expression of endothelin-1 (ET-1) and its specific receptors in the sensory retina after optic nerve injury.

Methods: The optic nerve of the right eye of Wistar rats was crushed. The sensory retinas were removed 1, 2, 4, 7, and 14 days after the surgery, and the amount of ET-1 in the retinas was measured by radioimmunoassay, and the mRNA levels of ET(A) and ET(B) receptors were determined by real-time PCR.

Endothelin-1 (ET-1) causes death of retinal neurons through activation of nitric oxide synthase (NOS) and production of superoxide anion.

Endothelin-1 (ET-1) is the most potent and long-acting vasoconstricting peptide presently known. In addition to its vascular effects, endothelin signaling pathway exists in the central nervous system (CNS), which is deeply related to neuronal degeneration. In the present study, we evaluated the effect of ET-1 on death of retinal neurons consisting mainly of amacrine cells, and its interaction with nitric oxide synthase (NOS) and superoxide production.

Angiotensin II receptor blocker inhibits abnormal accumulation of advanced glycation end products and retinal damage in a rat model of type 2 diabetes.

The effects of an angiotensin II receptor blocker (ARB) on the accumulation of one of advanced glycation end products (AGEs), pentosidine, expression of vascular endothelial growth factor (VEGF) and retinal function were investigated in Spontaneously Diabetic Torii (SDT) rats. Candesartan, an ARB, was administered to SDT rats from 10 to 44 weeks of age and the results compared with untreated SDT rats and SD rats. Electroretinograms (ERGs) were recorded to evaluate retinal function.

High infusion pressure in conjunction with vitreous surgery alters the morphology and function of the retina of rabbits.

Purpose: To investigate the effects of high infusion pressure in conjunction with pars plana vitrectomy (PPV) on retinal morphology and function in rabbits.

Methods: Pars plana vitrectomy was performed under urethane (0.8 mg/kg) anaesthesia in the right eye of albino rabbits following phacoemulsification and aspiration (PEA).

Effects of culture conditions on heterogeneity and the apical junctional complex of the ARPE-19 cell line.

Purpose: ARPE-19 is a spontaneously transformed cell line of human RPE that is widely studied. This report examines its suitability for studying the tight junctions of the RPE.

Methods: ARPE-19 was maintained in standard medium or one of three reduced-serum medium formulations.

Expression of JAM-A, AF-6, PAR-3 and PAR-6 during the assembly and remodeling of RPE tight junctions.

The tight junctions of the endothelial and epithelial regions of the blood-brain barrier are regulated by interactions with the neighboring tissue. We examined how the neural retina regulates the assembly of tight junctions in the retinal pigment epithelium (RPE). The proteins JAM-A, AF-6, PAR-3 and PAR-6 have been implicated in the assembly of other epithelial tight junctions.

Endothelin-1 enhances glutamate-induced retinal cell death, possibly through ETA receptors.

Purpose: To determine the modification of the glutamate-induced death of retinal neurons by endothelin (ET)-1.

Methods: Cultured retinal neurons from fetal rats were exposed to glutamate (1.0 mM) alone or glutamate with ET-1 (10(-10)-10(-7)M) for 10 minutes.

The apical and basal environments of the retinal pigment epithelium regulate the maturation of tight junctions during development.

A culture model has been established to study the gradual development of tight junctions during the embryogenesis of the chick retinal pigment epithelium. This study asks how closely the culture model reflects normal development and how the composition, structure and function of embryonic tight junctions are affected by the apical and basal environments. The study focused on the expression of claudins, the fine-structure of tight junctional strands and the transepithelial electrical resistance.