Protective Effects of Selectin Ligands/Inhibitor (SKK-60060) against Retinal Ischemia-Reperfusion Injury

Matsubara, Akiko; Tomida, Kazuyuki; Matsuda, Yoshito; Tamai, Kazushi; Tashita, Akira; Jomori, Takahito; Tsujikawa, Akitaka; Ogura, Yuichiro

doi:10.1006/exer.2000.0880

Cited by 16 publications

(18 citation statements)

References 38 publications

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“…Leukocytes are thought to play a significant role in ischemia-reperfusion injury, 1 because their accumulation results in tissue injury by impeding blood flow or by producing superoxide radicals 2 and inflammatory cytokines. 3 In our previous study using this model, we demonstrated that rolling and accumulated leukocytes were present in the retina, as 10 Pitavastatin Improved Leukocyte Dynamics in Retina observed by acridine orange digital fluorography, 4,5 and that mRNA expression of the leukocyte adhesion molecules P-selectin and intercellular adhesion molecule-1 (ICAM-1) was significantly increased. 6 Inhibition of selectin or ICAM-1 have been suggested as a possible treatment for ischemia-reperfusion injury, 7−9 and we have demonstrated that selectin inhibitor attenuates leukocyte rolling, accumulation, and subsequent tissue injury after ischemia-reperfusion in the rat retina.…”

Section: Introductionmentioning

confidence: 95%

Pitavastatin Attenuates Leukocyte-Endothelial Interactions Induced by Ischemia-Reperfusion Injury in the Rat Retina

Miyaki

Matsubara

Nishiwaki

et al. 2009

Current Eye Research

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Section: Introductionmentioning

confidence: 95%

Pitavastatin Attenuates Leukocyte-Endothelial Interactions Induced by Ischemia-Reperfusion Injury in the Rat Retina

Miyaki

Matsubara

Nishiwaki

et al. 2009

Current Eye Research

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“…On the basis of the results of these experiments, many investigators have studied various agents that can attenuate tissue damage by suppressing leukocyte-endothelial interactions in the postischemic retina. Antithrombin III [83,84], tacrolimus (FK506) [85], argatroban (direct thrombin inhibitor) [86], statin [87,88], Rho-associated protein kinase inhibitor [89], superoxide dismutase [90], thalidomide [91], selectin ligands/inhibitor (SKK-60060) [92], triamcinolone acetonide [93], ischemic preconditioning [94,95], platelet depression [81], and 17β-estradiol [96] are reported to reduce leukocyte accumulation in the postischemic retina and thereby reduce neural damage.…”

Section: Leukocyte-endothelial Interactions In Pathological Conditionsmentioning

confidence: 99%

Evaluation of Leukocyte-Endothelial Interactions in Retinal Diseases

Tsujikawa

Ogura

2011

Ophthalmologica

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Purpose: We reviewed various methodologies for studying leukocyte-retinal endothelial interactions in vivo, and summarized the information obtained from studies employing these methods. Procedures: Fluorescence dye-enhanced scanning laser ophthalmoscopy facilitates study of leukocyte-cell interactions in the retinal microcirculation. Results: Various methods such as adaptive optics scanning laser ophthalmoscopy (AO-SLO), acridine orange digital angiography, and intravital microscopy provided evidence of the mechanisms of leukocyte recruitment in the retina and of their importance in the pathogenesis of various retinal diseases. Conclusions: Leukocyte behavior can be easily examined in the retina in vivo because the optical media is transparent. SLO substantially contributes to visualizing leukocyte-endothelial interactions in retinal vessels, although most of the methods employing SLO could only be used for animal studies. AO-SLO noninvasively demonstrates the movement of each leukocyte in the parafoveal capillaries in humans. Message: AO-SLO could be useful in investigating the leukocyte-retinal endothelial interactions in various diseases in humans.

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“…[18][19][20]22 There have been a substantial number of studies that have examined the mechanisms responsible for retinal ischemia-reperfusion injury. The findings of these studies have demonstrated the involvement of a variety of factors including glutamate, 6,23 free radicals, 24 inflammatory adhesion molecules, 25 nitric oxide, 26 and cytokines. 27 In addition, it has also been reported that the neuronal damage that develops after ischemia-reperfusion injury is primarily caused by glutamate-mediated signaling that occurs especially via the NMDA receptor.…”

Section: Discussionmentioning

confidence: 99%

The Relationship Between the Renin-Angiotensin–Aldosterone System and NMDA Receptor-Mediated Signal and the Prevention of Retinal Ganglion Cell Death

Kobayashi

Hirooka

Ono

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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Citation: Kobayashi M, Hirooka K, Ono A, Nakano Y, Nishiyama A, Tsujikawa A. The relationship between the renin-angiotensin-aldosterone system and NMDA receptormediated signal and the prevention of retinal ganglion cell death. Invest Ophthalmol Vis Sci. 2017;58:139758: -140358: . DOI:10.1167 PURPOSE. Excitotoxicity, which is due to glutamate-induced toxic effects on the retinal ganglion cell (RGC), is one of several mechanisms of RGC loss. The renin-angiotensinaldosterone system (RAAS) has also been implicated in RGC death. Therefore, it is important to determine the exact relationship between the RAAS and N-methyl-d-aspartate (NMDA) receptor-mediated signal in order to prevent RGC death.METHODS. N-methyl-d-aspartate or aldosterone was injected into the vitreous body. After intravitreal injection of NMDA or aldosterone, animals were treated with spironolactone or memantine. Retinal damage was evaluated by measuring the number of RGCs at 4 weeks after local administration of aldosterone or at 2 weeks after local administration of NMDA. Vitreous humor levels of aldosterone were measured using enzyme immunoassay kits. RESULTS.A significantly decreased number of RGCs were observed after intravitreal injection of NMDA. Although spironolactone did not show any neuroprotective effects, memantine significantly reduced NMDA-induced degeneration in the retina. Furthermore, a significant decrease in the number of RGCs was observed after an intravitreal injection of aldosterone. While memantine did not exhibit any neuroprotective effects, spironolactone caused a significant reduction in the aldosterone-induced degeneration in the retina. There was no change in the aldosterone concentration in the vitreous humor after an NMDA injection.CONCLUSION. Our findings indirectly show that there is no relationship between the RAAS and NMDA receptor-mediated signal with regard to RGC death.Keywords: aldosterone, retinal ganglion cell, NMDA, glutamate W ithin the central nervous system, including the retina, glutamate functions as a major excitatory neurotransmitter. [1][2][3] Various diseases of the eye, which include glaucoma 4,5 and retinal ischemia, 6,7 have been shown to be associated with the glutamate receptor-mediated excitotoxicity. Glutamate excitotoxicity triggered by overactivation of the N-methyl-Daspartate (NMDA) receptors may be a potential risk factor for retinal ganglion cell (RGC) death.8 Indeed, it has been reported in an animal model that there is a decrease in the RGCs after an intravitreal injection of NMDA.9 One of the NMDA antagonists that has been demonstrated to have therapeutic potential against several central nervous system disorders is memantine (1-amino-3,5-dimethyladamantane). 10 Previous studies examined the use of memantine in several animal models of glaucoma and reported finding that this antagonist might possibility provide neuroprotection, although it was not successful in recent clinical trials. [11][12][13] Since multiple mechanisms can to lead to RGC death, this suggests that a neuroprotectant w...

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Protective Effects of Selectin Ligands/Inhibitor (SKK-60060) against Retinal Ischemia-Reperfusion Injury

Cited by 16 publications

References 38 publications

Pitavastatin Attenuates Leukocyte-Endothelial Interactions Induced by Ischemia-Reperfusion Injury in the Rat Retina

Pitavastatin Attenuates Leukocyte-Endothelial Interactions Induced by Ischemia-Reperfusion Injury in the Rat Retina

Evaluation of Leukocyte-Endothelial Interactions in Retinal Diseases

The Relationship Between the Renin-Angiotensin–Aldosterone System and NMDA Receptor-Mediated Signal and the Prevention of Retinal Ganglion Cell Death

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