H2O2-induced egr-1, fra-1, and c-jun gene expression is mediated by tyrosine kinase in aortic smooth muscle cells

Jin, Najia; Hatton, Nathan; Harrington, Maureen A.; Xia, Xiaolin; Larsen, Steve H; Rhoades, Rodney A.

doi:10.1016/s0891-5849(00)00376-2

Cited by 44 publications

(26 citation statements)

References 37 publications

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“…It has been reported that the EGFR (10,50,63,72) and PDGFR (18,28,42) participate in signaling events in response to oxidative injury. Because Gab1 is tyrosine phosphorylated after EGF (21,21) or PDGF addition (47), we sought to investigate the role of these receptors in Gab1 phosphorylation after H 2 O 2 stimulation.…”

Section: Resultsmentioning

confidence: 99%

“…Alternatively, there may be an attempt to adjust ROS levels, or in cases of sufficient damage, apoptosis is initiated to eliminate the damaged cells. The stress-induced proteins that are activated include tyrosine kinases such as epidermal growth factor (EGF) receptor (EGFR) (10,50,63,72), platelet-derived growth factor (PDGF) receptor (PDGFR) (18,28,42), and Src (1,37,38,48,64,69) and downstream pathways such as extracellular signal-regulated kinase (ERK) (20), c-Jun N-terminal kinase (JNK) (6,52), p38 (11), phosphatidylinositol 3-kinase (PI3K), AKT (33,63), the nuclear factor (NF)-B system (27), p53 activation (9,23,29), and the heat shock response (43,66). In general, the heat shock response, ERK, PI3K/AKT, and NF-B signaling pathways are prosurvival responses, whereas p53, JNK, and p38 activation is associated with apoptosis; however, exceptions should be considered a consequence of cellular specificity.…”

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confidence: 99%

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Gab1 Is an Integrator of Cell Death versus Cell Survival Signals in Oxidative Stress

Holgado-Madruga

Wong

2003

Molecular and Cellular Biology

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Upon the addition of different growth factors and cytokines, the Gab1 docking protein is tyrosine phosphorylated and in turn activates different signaling pathways. On the basis of the large body of evidence concerning cross talk between the signaling pathways activated by growth factors and oxidative stress, we decided to investigate the role of Gab1 in oxidative injury. We stimulated wild-type mouse embryo fibroblasts (MEF) or MEF with a homozygous deletion of the Gab1 gene (؊/؊ MEF) with H 2 O 2 . Our results show that Gab1 is phosphorylated in a dose-and time-dependent manner after H 2 O 2 triggering. Gab1 then recruits molecules such as SHP2, phosphatidylinositol 3-kinase (PI3K), and Shc. Gab1 phosphorylation is sensitive to the Src family kinase inhibitor PP2. Furthermore, we demonstrate that Gab1 is required for H 2 O 2 -induced c-Jun N-terminal kinase (JNK) activation but not for ERK2 or p38 activation. Reconstitution of Gab1 in ؊/؊ MEF rescues JNK activation, and we find that this is dependent on the SHP2 binding site in Gab1. Cell viability assays reveal that Gab1 has a dual role in cell survival: a positive one through its interaction with PI3K and a negative one through its interaction with SHP2. This is the first report identifying Gab1 as a component in oxidative stress signaling and one that is required for JNK activation.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Gab1 Is an Integrator of Cell Death versus Cell Survival Signals in Oxidative Stress

Holgado-Madruga

Wong

2003

Molecular and Cellular Biology

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“…The activation of MAPK is associated with VSMC proliferation due to stimulating the expression of downstream growthresponsive genes c-Jun, c-Fos and Elk-1, subsequently increasing DNA synthesis of VSMCs [11,12]. The c-Jun expression and activity are partly regulated by MAPK, and c-Jun is a major component of transcription factor AP-1 [20,21].…”

Section: Discussionmentioning

confidence: 99%

Roscovitine inhibits ERK1/2 activation induced by angiotensin II in vascular smooth muscle cells

Han

Zheng

et al. 2007

FEBS Letters

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Roscovitine is a potent CDK inhibitor often used as a biological tool in cell-cycle studies, but its working mechanism and real targets in vascular smooth muscle cells (VSMCs) remain unclear. In this study, we observed that ERK1/2 phosphorylation induced by Ang II was abrogated by pretreating VSMCs with roscovitine for 15 h. Pretreating VSMCs with roscovitine also inhibited Ang II-induced c-Jun expression and phosphorylation. We further demonstrated that roscovitine could suppress the DNA binding activity of c-Jun and activation of angiotensinogen promoter by Ang II. These results suggest that roscovitine represses Ang II-induced angiotensinogen expression by inhibiting activation of ERK1/2 and c-Jun.

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“…9,19 The present study addressed the hypothesis that extracorpuscular free heme upregulates Egr-1 and its downstream targets in vascular tissue as part of the immediate cellular response to oxidative stress, the deregulation of which may contribute to inflammatory vascular diseases such as atherosclerosis. We examined the regulation of Egr-1 by hemin (ferriprotoporphyrin IX, the oxidized form of heme) in human vascular SMCs and present evidence that Egr-1 is upregulated by hemin in a redox-sensitive manner via the mitogen activated protein kinase (MAPK) ERK-1/2 and the transcription factors SRF, Elk-1, and NF-B.…”

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confidence: 99%

Hemin Upregulates Egr-1 Expression in Vascular Smooth Muscle Cells via Reactive Oxygen Species ERK-1/2–Elk-1 and NF-κB

Hasan

Schafer

2008

Circulation Research

109

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Abstract-Reactive oxygen species (ROS) and oxidant stress are important mediators of cardiovascular pathologies including atherosclerosis. One source of ROS in the vasculature is free heme released from hemoglobin. Because Egr-1, the regulator of cell proliferation and apoptosis, is also induced by oxidant stress and is likewise implicated in atherosclerosis, we examined the regulation of Egr-1 by heme in vascular smooth muscle cells (SMCs). Hemin increased Egr-1 expression (mRNA, protein) within 30 minutes and ERK-1/2 phosphorylation and nuclear translocation within 5 minutes. Inhibiting hemin-induced ERK-1/2 activation by U0126 (MAPK-inhibitor), the antioxidant N-acetyl cysteine, the NADPH oxidase inhibitors apocynin and diphenyleneiodonium chloride, the superoxide scavenger tiron, or tricarbonyldichlororuthenium (

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H2O2-induced egr-1, fra-1, and c-jun gene expression is mediated by tyrosine kinase in aortic smooth muscle cells

Cited by 44 publications

References 37 publications

Gab1 Is an Integrator of Cell Death versus Cell Survival Signals in Oxidative Stress

Gab1 Is an Integrator of Cell Death versus Cell Survival Signals in Oxidative Stress

Roscovitine inhibits ERK1/2 activation induced by angiotensin II in vascular smooth muscle cells

Hemin Upregulates Egr-1 Expression in Vascular Smooth Muscle Cells via Reactive Oxygen Species ERK-1/2–Elk-1 and NF-κB

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