Current eye research
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Current eye research · Apr 2009
Elevated Expression of indoleamine 2,3-dioxygenase (IDO) and accumulation of kynurenic acid in the pathogenesis of STZ-induced diabetic cataract in Wistar rats.
Glycated lens proteins are capable of producing reactive oxygen species (ROS), which, in turn, can oxidize tryptophan (Trp) into kynurenines. Indoleamine 2,3-dioxygenase (IDO), which is expressed in many tissues and which is inducible by interferon-gamma (IFN-gamma), is able to oxidize Trp into kynurenines. These kynurenines can modify lens proteins and, in fact, kynurenine adducts are markedly increased in lenses with age-related nuclear cataract. Therefore, it has been suggested that lenticular IDO is involved in diabetic cataractogenesis. The aim of the present study was to examine the possible role(s) of IDO in streptozotocin (STZ)-induced diabetic cataract in rats. ⋯ Production of IDO was induced in STZ-induced diabetic cataractous lenses, possibly by locally produced IFN- gamma. IDO-mediated oxidation of Trp may partly explain the increase in lens KYNA and may thus be implicated in cataractogenesis in concert with the non-enzymic oxidation of Trp by glycated lens proteins.
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Current eye research · Jul 2008
Tetrandrine suppresses activation of human subconjunctival fibroblasts in vitro.
To investigate the effect of tetrandrine on activation of human subconjunctival fibroblasts (SCFs) in vitro. ⋯ Tetrandrine suppresses Smad2 signal and fibrogenic responses in SCFs in association with Smad7 up-regulation, suggesting its potential therapeutic value to prevent excess scarring/fibrosis in conjunctiva following trabeculectomy or in patients with severe conjunctival inflammation.
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Current eye research · Sep 2007
Randomized Controlled TrialEffect of dexamethasone eyedrops on blood glucose profile.
To evaluate the effect of dexamethasone eyedrops on blood glucose. ⋯ Postoperative dexamethasone eyedrops have a greater effect on the blood glucose profile of diabetic patients than on nondiabetic patients. Clinicians should be alerted to this risk and may initiate appropriate follow-up in this patient subgroup.
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Current eye research · Jun 2007
Protein kinase C-gamma activation in the early streptozotocin diabetic rat lens.
The purpose of this study is to demonstrate the early activation of the protein kinase C-gamma (PKC-gamma) pathway in the streptozotocin (STZ)-induced diabetic rat lens. ⋯ Early activation of PLC-gamma 1 and elevated DAG were observed within VHG diabetic lenses. These were correlated with activation of PKC-gamma, phosphorylation of Cx43 on Ser368, and inhibition of dye transfer. Abnormal signaling from PKC-gamma to Cx43 in the epithelial cells/early fiber cells, observed within VHG diabetic lenses, may be responsible for fiber cell damage deeper in the lens cortex.
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Current eye research · Dec 2006
Involvement of MAPKs in endostatin-mediated regulation of blood-retinal barrier function.
This study aimed to evaluate the effects of endostatin on tight junction (TJ) integrity in retinal microvascular endothelial cells (RMECs) in vitro and in vivo. Moreover, it was hypothesized that endostatin-induced occludin upregulation regulated VEGF165-mediated increases in endothelial cell permeability and involved activation of the MAPK signaling cascade. Endostatin is a 20-kDa fragment of collagen XVIII that has been shown to be efficacious in the eye by preventing retinal neovascularization. Endostatin is a specific inhibitor of endothelial cell proliferation, migration, and angiogenesis and has been reported to reverse VEGF-mediated increases in vasopermeability and to promote integrity of the blood-retinal barrier (BRB). In order to determine the mechanism of endostatin action on BRB integrity, we have examined the effects of endostatin on a number of intracellular pathways implicated in endothelial cell physiology. ⋯ Occludin is important for the maintenance of tight junction integrity in vivo. In a p38 MAPK and ERK1/ERK2 dependent manner, endostatin was shown to upregulate the levels of expression of the tight junction protein occludin. Inhibition of these key MAPK components may prevent endostatin's ability to decrease VEGF165-induced paracellular permeability.