Ets-2 Is Induced by Oxidative Stress and Sensitizes Cells to H2O2-Induced Apoptosis: Implications for Down's Syndrome

Sanij, Elaine; Hatzistavrou, Tanya; Hertzog, Paul J.; Kola,; Wolvetang, EJ

doi:10.1006/bbrc.2002.6411

Cited by 5 publications

(7 citation statements)

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“…Ets-2 is active in its monomeric form and interacts with other transcription factors binding to adjacent sites to activate transcription. Ets-2 activation induces neuronal apoptosis in response to oxidative stress (30,31) but rescues macrophages from stress induced by colony-stimulating factor 1 depletion through a Bcl-xL-dependent mechanism (26). In differentiated myeloid cells, such as human U937 and HL60 cells, Ets-2 and Bcl-xL are coexpressed (26).…”

Section: Discussionmentioning

confidence: 99%

“…Glial activation and Bcl-xL expression in transgenic ALS (G93A) mice. A) Age-dependent(30, 70, 90, and 120 days) increase of GFAP immunoreactivity in the ventral horn of lumbar spinal cord sections in G93A mice (e-h) but not in wild-type (WT) littermate control mice (a-d). B) Age-dependent increase of Bcl-xL immunoreactivity in the ventral horn of lumbar spinal cord sections in G93A mice (eЈ-hЈ) compared with WT mice (aЈ-dЈ).…”

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confidence: 99%

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Activation of Ets‐2 by oxidative stress induces Bcl‐xL expression and accounts for glial survival in amyotrophic lateral sclerosis

Lee

Kannagi²,

Ferrante

et al. 2009

FASEB j.

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Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by selective degeneration of motor neurons and glial activation. Cell-specific transcriptional regulation induced by oxidative stress may contribute to the survival and activation of astrocytes in the face of motor neuron death. In the present study, we demonstrate an age-dependent increase in Bcl-xL and Ets-2 immunoreactivity that correlates with an increase of glial fibrillary acidic protein (GFAP)-positive cells in the ventral horn of the spinal cord in both ALS transgenic mice [mutant SOD1 (G93A)] and affected humans. Chromatin immunoprecipitation (ChIP) analysis verified that Ets-2 preferentially occupies the Ets-2 binding element in the promoter of Bcl-xL in primary astrocytes under oxidative stress conditions as well as in G93A spinal cords. Ets-2 small-interfering RNA down-regulated the transcriptional activity of Bcl-xL. In primary glial cultures, Bcl-xL overexpression and mutant SOD1 (G93A) both conferred resistance to oxidative stress-induced cell death. Our findings suggest that Ets-2 transcription factor activation of Bcl-xL gene may protect glia from constitutive oxidative stress that is thought to be a key mechanism contributing to the pathogenesis of ALS. This survival pathway may contribute to the glial survival and activation seen in the spinal cord of ALS patients.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Activation of Ets‐2 by oxidative stress induces Bcl‐xL expression and accounts for glial survival in amyotrophic lateral sclerosis

Lee

Kannagi²,

Ferrante

et al. 2009

FASEB j.

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“…Nonetheless, from murine promoter analysis, binding sites for transcription factors Sp-1, Ap-2, and Ets reside in both ␣ 7 -and ␣ v -promoters (23,51), and these binding sites have been shown to be redox sensitive (17,34,39), which suggests the possibility of common regulatory pathways involved in increased ␣ 7 -and ␣ v -integrin levels.…”

Section: Discussionmentioning

confidence: 99%

“…Five putative Sp-1 binding sites, eight consensus E-boxes providing the binding sites for basic helixloop-helix (bHLH), two Ap-1 binding sites, one Ap-2 binding site, and one Ets binding site have been identified within the 5Ј-flanking region. Although it is not known whether these elements and their transcription factors play a role in AAMinduced ␣ 7 -expression in VSMCs, Ap-1, Ap-2, and Ets are activated by reactive oxygen species (17,18,39). Sp-1 and bHLH proteins have also been implicated in redox signaling in VSMCs (34).…”

Section: Discussionmentioning

confidence: 99%

Regulation of α₇-integrin expression in vascular smooth muscle by injury-induced atherosclerosis

Chao¹,

Meininger²,

Patterson³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Injury of vascular smooth muscle cells (VSMCs) by allylamine (AAM) leads to phenotypic changes associated with atherogenic progression including increased proliferation, migration, and alterations in cell adhesion. In the present study, the relationship between AAM-induced vascular injury and expression of the alpha(7)-integrin subunit was investigated. The alpha(7)-mRNA and protein expression were examined using real-time RT-PCR, fluorescence-activated cell sorting analysis (FACS), immunohistochemistry, and immunoblotting. In cultured VSMCs from aortas of AAM-treated rats (70 mg/kg for 20 days), alpha(7)-mRNA levels were increased more than twofold compared with control cells. No change was seen in beta(1)-integrin expression. FACS analysis revealed increased cell surface expression of alpha(7)-protein (25 +/- 9%; *P < 0.05). AAM treatment of naive VSMCs enhanced alpha(7)-mRNA expression (2.4 +/- 0.7-fold, mean +/- SE; *P < 0.05). The increased alpha(7)-mRNA expression was attenuated by the amine oxidase inhibitor semicarbazide and the antioxidant pyrrolidine dithiocarbamate, which confirms a role for oxidative stress in modulating alpha(7)-expression. In vivo alpha(7)-mRNA and protein expression were enhanced in the aortas of AAM-treated rats. In addition, increased alpha(7)-integrin expression facilitated AAM VSMC adhesion to laminin more efficiently compared with control (51 +/- 2%; *P < 0.05). Chemical injury induced by AAM significantly enhances alpha(7)-integrin expression in VSMCs. These findings implicate for the first time the expression of alpha(7)-integrin during the response of VSMCs to vascular injury.

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“…Other evidence suggests that ETS2 over‐expression in transgenic mice and in Down syndrome predisposes apoptosis via the p53 pathway 52. ETS2 is also induced by oxidative stress and sensitizes cells to hydrogen peroxide induced apoptosis 53. Together, these studies suggest that increased ROS production on the background of increased ETS2 expression and imbalance of the antioxidant enzymes SOD1/GPX+ catalase such as occurs in Down syndrome may prime the cells for spontaneous apoptosis and thereby drug induced apoptosis.…”

Section: Introductionmentioning

confidence: 97%

Real-time evaluation of the hemodynamic effects of atrial septal defect closure in adults with left ventricular dysfunction

Tomai

Andò

Paulis

et al. 2004

Cathet. Cardiovasc. Intervent.

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Transcatheter closure of atrial septal defects with left-to-right shunt induces an abrupt overload of the left ventricle that may cause acute heart failure in patients with left ventricular dysfunction. We report two cases of ostium secundum atrial septal defects associated with left ventricular dysfunction of different etiology. The hemodynamic evaluation of left ventricular function during transient abolition of the shunt with the sizing balloon of the Amplatzer system helped to establish the most correct therapeutic strategy.

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Ets-2 Is Induced by Oxidative Stress and Sensitizes Cells to H2O2-Induced Apoptosis: Implications for Down's Syndrome

Cited by 5 publications

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Activation of Ets‐2 by oxidative stress induces Bcl‐xL expression and accounts for glial survival in amyotrophic lateral sclerosis

Activation of Ets‐2 by oxidative stress induces Bcl‐xL expression and accounts for glial survival in amyotrophic lateral sclerosis

Regulation of α₇-integrin expression in vascular smooth muscle by injury-induced atherosclerosis

Real-time evaluation of the hemodynamic effects of atrial septal defect closure in adults with left ventricular dysfunction

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Ets-2 Is Induced by Oxidative Stress and Sensitizes Cells to H2O2-Induced Apoptosis: Implications for Down's Syndrome

Cited by 5 publications

References 0 publications

Activation of Ets‐2 by oxidative stress induces Bcl‐xL expression and accounts for glial survival in amyotrophic lateral sclerosis

Activation of Ets‐2 by oxidative stress induces Bcl‐xL expression and accounts for glial survival in amyotrophic lateral sclerosis

Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis

Real-time evaluation of the hemodynamic effects of atrial septal defect closure in adults with left ventricular dysfunction

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Regulation of α₇-integrin expression in vascular smooth muscle by injury-induced atherosclerosis