2007
DOI: 10.1167/iovs.07-0112
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Inducible Nitric Oxide Synthase Isoform Is a Key Mediator of Leukostasis and Blood-Retinal Barrier Breakdown in Diabetic Retinopathy

Abstract: These results indicate that the iNOS isoform plays a predominant role in leukostasis and BRB breakdown. The mechanism involves ICAM-1 upregulation and tight junction protein downregulation.

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Cited by 224 publications
(171 citation statements)
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References 38 publications
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“…NO is also reported to be involved in the breakdown of the BRB [55,56]. NO is primarily synthesized from L-arginine by the NOS enzymes and is known to mediate neuronal communication as well vasodilatation.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…NO is also reported to be involved in the breakdown of the BRB [55,56]. NO is primarily synthesized from L-arginine by the NOS enzymes and is known to mediate neuronal communication as well vasodilatation.…”
Section: Introductionmentioning
confidence: 99%
“…Joussen et al [29] demonstrated that the increased production of VEGF could induce eNOS expression in the retina which could result in increased NO. NO derived from iNOS and eNOS was further found to facilitate BRB disruption by increasing ICAM-1 expression in the retinal endothelial cells which could promote leukocyte adhesion [55,29]. The potential of NO in mediating BRB breakdown was further evident with its ability to reduce the expression of TJ molecules such as ZO-1 and occludin [55].…”
Section: Introductionmentioning
confidence: 99%
“…SST may be involved in regulating the permeability of endothelial and epithelial barriers. SST inhibits nitric oxide production, 16,17 which was found to be involved in disruption of tight junctions in Chinese hamster ovary endothelial cells. 18 The human receptor of SST 3, a subtype of SST receptor, physically interacts with an epithelial tight junction protein known as MUPP1 (multiple PDZ domain protein-1), which enables SST to regulate transepithelial permeability.…”
Section: Discussionmentioning
confidence: 99%
“…In the retina, iNOS is sensitive to hyperglycemia and responsible for overproduction of NO (30,31). The resulting surplus of NO is either quenched by advanced glycation end products (AGEs) or leads, through the reaction with superoxide, to the formation of peroxynitrite with subsequent nitrosylation of proteins, lipids, and DNA.…”
Section: Retinopathymentioning
confidence: 99%