Short-Term Hyperhomocysteinemia-Induced Oxidative Stress Activates Retinal Glial Cells and Increases Vascular Endothelial Growth Factor Expression in Rat Retina

Lee, Insun; Lee, Hwayoung; Kim, Ji-Myung; Chae, Eun Hye; Kim, Soo Jung; Chang, Namsoo

doi:10.1271/bbb.60657

Cited by 33 publications

(20 citation statements)

References 42 publications

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“…Although TAC was associated with TBARS by regression analysis, it was not found to be an independent risk factor for the disease. While Lee et al 38 reported on homocysteine-induced oxidative stress in retinal glial cells, this is the first report on the increase in oxidative stress of homocysteine in augmenting the oxidative stress in retinal endothelilal cells. Homocysteine is reported as a potent excitatory neurotransmitter that acted via a N -methyl-d-aspartate receptor and leading to oxidative stress and endothelial dysfunction 39.…”

Section: Discussionmentioning

confidence: 66%

“…Homocysteine is reported as a potent excitatory neurotransmitter that acted via a N -methyl-d-aspartate receptor and leading to oxidative stress and endothelial dysfunction 39. Animal studies have revealed that the homocystine diet-fed group in rats showed higher plasma homocysteine, TBARS and lower plasma levels of retinol, α-tocopherol and retinal expression of SOD than those of the controls 38. Microarray analysis in human umbilical vein endothelial cells exposed to homocysteine in vitro revealed decreased expression of several antioxidant enzymes, including glutathione peroxidase, SOD, natural killer-enhancing factors and proliferation-associated glycoprotein 40.…”

Section: Discussionmentioning

confidence: 98%

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Homocysteine induces oxidative stress in young adult central retinal vein occlusion

et al. 2012

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 98%

Homocysteine induces oxidative stress in young adult central retinal vein occlusion

et al. 2012

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“…Homocysteine may affect retinal cells through increased oxidative stress (Lee et al 2007), and intravitreal homocysteine injections have been shown to be toxic to ganglion-cell neurons (Moore et al 2001). Homocysteine can damage neurons in several layers of rat retina in vitro (Viktorov et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Complete deficiency of methylenetetrahydrofolate reductase in mice is associated with impaired retinal function and variable mortality, hematological profiles, and reproductive outcomes

Lawrance

Racine

Deng

et al. 2010

J of Inher Metab Disea

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Severe deficiency of methylenetetrahydrofolate reductase (MTHFR) with homocystinuria can result in early demise or later-onset neurological impairment, including developmental delay, motor dysfunction, and seizures. We previously characterized BALB/c Mthfr (-/-)mice as a model for this disorder and have recently backcrossed the disrupted allele onto the C57Bl/6 background to examine the variable phenotypes in MTHFR deficiency. Compared with BALB/c Mthfr (-/-)mice, C57Bl/6 Mthfr (-/-)mice have enhanced survival rates (81% vs 26.5%). Four-day-old BALB/c mutant pups had lower body, brain, and spleen weights relative to their wild-type counterparts compared with C57Bl/6 mutants. Pregnant BALB/c Mthfr (+/-)mice had increased resorptions and embryonic delays compared with wild-type littermates, whereas these outcomes in C57Bl/6 c Mthfr (+/-)mice were similar to those of wild-type C57Bl/6 mice. BALB/c-mutant pups had altered hematological profiles (higher hematocrit, hemoglobin, and white blood cell counts, with lower platelet counts) compared with C57Bl/6 mutants. Mutants of both strains had similar degrees of hepatic steatosis, hepatic activity of betaine:homocysteine methyltransferase, and altered cerebellar histology. Electroretinograms (ERG) in C57Bl/6 Mthfr (-/-)mice revealed decreased amplitude of scotopic and photopic waves in 6-week-old mice, with normalized ERGs at 13 weeks. Plasma homocysteine was modestly higher in C57Bl/6 compared with BALB/c mice. Our results emphasize the variable presentation of MTHFR deficiency in different genetic backgrounds and suggest that plasma homocysteine is not a predictor of severity. In addition, our novel findings of decreased spleen weights, thrombocytopenia, and impaired retinal function warrant investigation in patients with severe MTHFR deficiency or other forms of homocystinuria.

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“…A recent study by Roybal et al 37 showed that Hcy increases the expression of VEGF in the retinal pigment epithelium line. An animal study 38 also found that hHcy increased VEGF inmunoreactivity in the retina of rats. Therefore, the hHcy was significantly associated with the wet AMD variety.…”

Section: Discussionmentioning

confidence: 87%

Effect of Pegaptanib and Ranibizumab on Plasma and Vitreous Homocysteine in Patients With Exudative Age-Related Macular Degeneration

Manresa

Mulero

Losada³

et al. 2015

Retina

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Short-Term Hyperhomocysteinemia-Induced Oxidative Stress Activates Retinal Glial Cells and Increases Vascular Endothelial Growth Factor Expression in Rat Retina

Cited by 33 publications

References 42 publications

Homocysteine induces oxidative stress in young adult central retinal vein occlusion

Homocysteine induces oxidative stress in young adult central retinal vein occlusion

Complete deficiency of methylenetetrahydrofolate reductase in mice is associated with impaired retinal function and variable mortality, hematological profiles, and reproductive outcomes

Effect of Pegaptanib and Ranibizumab on Plasma and Vitreous Homocysteine in Patients With Exudative Age-Related Macular Degeneration

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