Oxidative stress increases glyceraldehyde-3-phosphate dehydrogenase mRNA levels in isolated rabbit aorta

Ito, Yasushi; Pagano, Patrick J.; Tornheim, Keith; Brecher, Peter; Cohen, Richard A.

doi:10.1152/ajpheart.1996.270.1.h81

Cited by 44 publications

(33 citation statements)

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“…There was no change in expression of β-actin, but GAPDH showed a fourfold increase in expression in ischemic retinas of Sod1 −/− mice compared with those of Sod1 +/− that was blocked by antioxidants. This finding is consistent with previous reports showing that GAPDH is induced by hypoxia and oxidative stress, including inhibition of SOD1 (17,18).…”

Section: Resultssupporting

confidence: 94%

Vascular cell-adhesion molecule-1 plays a central role in the proangiogenic effects of oxidative stress

Dong

Shen²,

Zeng

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Oxidative stress exacerbates neovascularization (NV) in many disease processes. In this study we investigated the mechanism of that effect. Mice deficient in superoxide dismutase 1 (Sod1 −/− mice) have increased oxidative stress and show severe ocular NV that is reduced to baseline by antioxidants. Compared with wild-type mice with ischemic retinopathy, Sod1−/− mice with ischemic retinopathy had increased expression of several NF-κB-responsive genes, but expression of vascular cell-adhesion molecule-1 (Vcam1) was particularly high. Intraocular injection of anti-VCAM-1 antibody eliminated the excessive ischemia-induced retinal NV. Elements that contributed to oxidative stress-induced worsening of retinal NV that were abrogated by blockade of VCAM-1 included increases in leukostasis, influx of bone marrow-derived cells, and capillary closure. Compared with ischemia alone, ischemia plus oxidative stress resulted in increased expression of several HIF-1-responsive genes caused in part by VCAM-1-induced worsening of nonperfusion and, hence, ischemia, because anti-VCAM-1 significantly reduced the increased expression of all but one of the genes. These data explain why oxidative stress worsens ischemia-induced retinal NV and may be relevant to other neovascular diseases in which oxidative stress has been implicated. The data also suggest that antagonism of VCAM-1 provides a potential therapy to combat worsening of neovascular diseases by oxidative stress.age-related macular degeneration | diabetic retinopathy | reactive oxygen species

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Section: Resultssupporting

confidence: 94%

Vascular cell-adhesion molecule-1 plays a central role in the proangiogenic effects of oxidative stress

Dong

Shen²,

Zeng

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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“…Transcription levels of GAPDH vary among cell types (Barber et al 2005), developmental stages (Robert et al 2002) and experimental conditions (Ito et al 1996;Zhong and Simons 1999).These findings underline the priority of reference gene validation for each specific developmental stage and for each season. This report also raises concern as GAPDH has been generally used as an internal control gene in studies involving the effect of seasons on oocyte and embryo gene expression in cattle and buffaloes (Sakatani et al 2013;Yadav et al 2013).…”

Section: Discussionmentioning

confidence: 75%

Developmental competence and expression profile of genes in buffalo (Bubalus bubalis) oocytes and embryos collected under different environmental stress

et al. 2016

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The study examined the effects of different environmental stress on developmental competence and the relative abundance (RA) of various gene transcripts in oocytes and embryos of buffalo. Oocytes collected during cold period (CP) and hot period (HP) were matured, fertilized and cultured in vitro to blastocyst hatching stage. The mRNA expression patterns of genes implicated in developmental competence (OCT-4, IGF-2R and GDF-9), heat shock (HSP-70.1), oxidative stress (MnSOD), metabolism (GLUT-1), pro-apoptosis (BAX) and anti-apoptosis (BCL-2) were evaluated in immature and matured oocytes as well as in pre-implantation stage embryos. Oocytes reaching MII stage, cleavage rates, blastocyst yield and hatching rates increased (P \ 0.05) during the CP. In MII oocytes and 2-cell embryos, the RA of OCT-4, IGF-2R, GDF-9, MnSOD and GLUT-1 decreased (P \ 0.05) during the HP. In 4-cell embryos, the RA of OCT-4, IGF-2R and BCL-2 decreased (P \ 0.05) in the HP, whereas GDF-9 increased (P \ 0.05). In 8-to 16-cell embryos, the RA of OCT-4 and BCL-2 decreased (P \ 0. 05) in the HP, whereas HSP-70.1 and BAX expression increased (P \ 0.05). In morula and blastocyst, the RA of OCT-4, IGF-2R and MnSOD decreased (P \ 0.05) during the HP, whereas HSP-70.1 was increased (P \ 0.05). In conclusion, deleterious seasonal effects induced at the GVstage carry-over to subsequent embryonic developmental stages and compromise oocyte developmental competence and quality of developed blastocysts.

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“…For all mRNA analysis, 36b4 mRNA was used for normalization. The housekeeping gene Gapdh was also tested, but its expression showed alteration with the treatment (data not shown), probably related to reduction in oxidative stress induced by CB1R antagonism (Comelli et al 2010), pointing out that oxidative stress could increase Gapdh mRNA expression (Ito et al 1996).…”

Section: Resultsmentioning

confidence: 99%

Inhibition of cannabinoid CB1 receptor upregulates Slc2a4 expression via nuclear factor-κB and sterol regulatory element-binding protein-1 in adipocytes

Furuya

Poletto²,

Freitas³

et al. 2012

Journal of Molecular Endocrinology

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Evidences have suggested that the endocannabinoid system is overactive in obesity, resulting in enhanced endocannabinoid levels in both circulation and visceral adipose tissue. The blockade of cannabinoid receptor type 1 (CB1) has been proposed for the treatment of obesity. Besides loss of body weight, CB1 antagonism improves insulin sensitivity, in which the glucose transporter type 4 (GLUT4) plays a key role. The aim of this study was to investigate the modulation of GLUT4-encoded gene (Slc2a4 gene) expression by CB1 receptor. For this, 3T3-L1 adipocytes were incubated in the presence of a highly selective CB1 receptor agonist (1 mM arachidonyl-2 0 -chloroethylamide) and/or a CB1 receptor antagonist/inverse agonist (0 . 1, 0 . 5, or 1 mM AM251, 1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-1-piperidinyl-1H-pyrazole-3-carboxamide). After acute (2 and 4 h) and chronic (24 h) treatments, cells were harvested to evaluate: i) Slc2a4, Cnr1 (CB1 receptor-encoded gene), and Srebf1 type a (SREBP-1a type-encoded gene) mRNAs (real-time PCR); ii) GLUT4 protein (western blotting); and iii) binding activity of nuclear factor (NF)-kB and sterol regulatory element-binding protein (SREBP)-1 specifically in the promoter of Slc2a4 gene (electrophoretic mobility shift assay). Results revealed that both acute and chronic CB1 receptor antagonism greatly increased (w2 . 5-fold) Slc2a4 mRNA and protein content. Additionally, CB1-induced upregulation of Slc2a4 was accompanied by decreased binding activity of NF-kB at 2 and 24 h, and by increased binding activity of the SREBP-1 at 24 h. In conclusion, these findings reveal that the blockade of CB1 receptor markedly increases Slc2a4/GLUT4 expression in adipocytes, a feature that involves NF-kB and SREBP-1 transcriptional regulation.

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Oxidative stress increases glyceraldehyde-3-phosphate dehydrogenase mRNA levels in isolated rabbit aorta

Cited by 44 publications

References 0 publications

Vascular cell-adhesion molecule-1 plays a central role in the proangiogenic effects of oxidative stress

Vascular cell-adhesion molecule-1 plays a central role in the proangiogenic effects of oxidative stress

Developmental competence and expression profile of genes in buffalo (Bubalus bubalis) oocytes and embryos collected under different environmental stress

Inhibition of cannabinoid CB1 receptor upregulates Slc2a4 expression via nuclear factor-κB and sterol regulatory element-binding protein-1 in adipocytes

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