JunB Forms the Majority of the AP-1 Complex and Is a Target for Redox Regulation by Receptor Tyrosine Kinase and G Protein-coupled Receptor Agonists in Smooth Muscle Cells

Rao, Gadiparthi N.; Katki, Khurshed A.; Madamanchi, Nageswara R.; Wu, Yaxu; Birrer, Michael J.

doi:10.1074/jbc.274.9.6003

Cited by 107 publications

(88 citation statements)

References 62 publications

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“…After immunoprecipitation of nuclear extracts with anti-Ref-1 rab- AP-1, an inducible transcription factor that recognizes a palindromic sequence (5Ј-TGACTCA-3Ј, phorbol 12-O-tetradecanoate-13-acetate-responsive element), is a homodimeric or heterodimeric leucine zipper complex containing the products of the fos and jun protooncogenes (45). AP-1 has been identified as an intermediary in PDGF-induced proliferation of SMCs (34). The activity of AP-1 is controlled not only by transcriptional and posttranscriptional mechanisms via increased rates of synthesis and decreased rates of degradation of fos and jun mRNA species, but also by translational and posttranslational (phosphorylation and redox regulation) mechanisms (7,40,45) (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies (27,34,37,39) from our lab and others have shown that PDGF can activate NAD(P)H oxidase in SMCs to produce O 2 Ϫ ⅐. This growth factorinduced NAD(P)H oxidase-dependent reactive oxygen species (ROS) generation leads to activation of transcription factors such as AP-1 and, consequently, cell proliferation (14,22,34,39).…”

mentioning

confidence: 99%

“…This growth factorinduced NAD(P)H oxidase-dependent reactive oxygen species (ROS) generation leads to activation of transcription factors such as AP-1 and, consequently, cell proliferation (14,22,34,39). Although Ref-1 has been reported to be elevated in some cancers such as prostate, ovarian, and cervical cancer (25,30,48), and to be involved in inhibition of apoptosis (6), a potential role of Ref-1 in SMC proliferation has not been examined.…”

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confidence: 99%

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Redox factor-1 contributes to the regulation of progression from G₀/G₁ to S by PDGF in vascular smooth muscle cells

He¹,

Weintraub²,

Goswami³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Redox factor-1 contributes to the regulation of progression from G₀/G₁ to S by PDGF in vascular smooth muscle cells

He¹,

Weintraub²,

Goswami³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…In addition, thrombin stimulates ERK1/2, p38 mitogen activated protein kinase (p38MAPK) and JNK signaling, leading to induction of c-Fos and Jun-B, which combine to activate AP-1-mediated gene expression. Activation of all of these pathways is inhibited by NAC or DPI (Rao et al 1999). Similar to the signaling pathways utilized by AngII, catecholamines stimulate VSMC proliferation by ROS-dependent transactivation of the EGF receptor ).…”

Section: Vascular Smooth Muscle Proliferationmentioning

confidence: 99%

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Papaharalambus

Griendling

2007

Trends in Cardiovascular Medicine

291

224

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The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species, produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.The fundamental processes underlying the development of vascular diseases such as atherosclerosis, restenosis and hypertensive vascular remodeling have their origins in an initial insult to the vessel wall. Such an insult may arise from mechanical disruption that occurs during percutaneous coronary angioplasty or at regions of oscillatory shear stress, or it can result from biological causes, such as hypercholesterolemia, excess free radicals, diabetes, increased concentrations of plasma homocysteine, or infectious agents. Injury promotes disruption of the homeostatic mechanisms of the endothelial protective barrier, changing its natural properties, increasing its adhesiveness to leukocytes and altering its permeability. This endothelial dysfunction also leads to the formation of vasoactive molecules, which in turn induce inflammatory genes, inactivate nitric oxide (NO • ) and its protective functions, and activate matrix metalloproteinases, leading to extracellular matrix remodeling, and increased smooth muscle cell (VSMC) growth, migration and proliferation. Each of these processes contributes to thickening of the vessel wall or the formation of lesions that can lead to hypertension, acute myocardial infarction and stroke. Reactive Oxygen Species and Vascular InjuryIn the past decade a staggering amount of evidence implicates a common denominator, reactive oxygen species (ROS), in the development of most cardiovascular diseases (Figure 1). Superoxide (O 2 •− ) and hydrogen peroxide (H 2 O 2 ) are two of the most biologically important ROS in the cardiovascular system, and are produced in vascular cells by a number of oxidases, including the NADPH oxidases (Nox) and xanthine oxidase, lipoxygenases, cytochrome p450,

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“…JunB has been shown to dimerize and transactivate AP-1 genes but can also act as a negative regulator of c-Jun for some genes (10,37). In cultured VSMCs, JunB has been detected in active AP-1 complexes in cells responding to receptor tyrosine kinase and G protein-coupled receptor agonists, and its induction is related to the production of reactive oxygen species (41). These findings together with our findings that Jun-and CREB-regulated genes are overrepresented in cerebral arteries from hypertensive animals indicate that signaling through AP-1 and CRE promoter elements may be particularly relevant in the arterial remodeling response.…”

Section: Discussionmentioning

confidence: 99%

Genes overexpressed in cerebral arteries following salt-induced hypertensive disease are regulated by angiotensin II, JunB, and CREB

Rose¹,

Bond²,

Tighe³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Rose P, Bond J, Tighe S, Toth MJ, Wellman TL, de Montiano EM, Lewinter MM, Lounsbury KM. Genes overexpressed in cerebral arteries following salt-induced hypertensive disease are regulated by angiotensin II, JunB, and CREB. Am J Physiol Heart Circ Physiol 294: H1075-H1085, 2008. First published December 21, 2007 doi:10.1152/ajpheart.00913.2007.-Although changes in gene expression are necessary for arterial remodeling during hypertension, the genes altered and their mechanisms of regulation remain uncertain. The goal of this study was to identify cerebral artery genes altered by hypertension and define signaling pathways important in their regulation. Intact cerebral arteries from Dahl salt-sensitive normotensive and hypertensive high-salt (HS) rats were examined by immunostaining, revealing an increased phosphorylation of extracellular signalregulated kinase 1/2 (ERK1/2) and expression of the proliferative marker Ki-67 in arteries from hypertensive animals. Arterial RNA analyzed by microarray and validated with RT-quantitative PCR revealed that jun family member junB and matricellular genes plasminogen activator inhibitor-1 (PAI-1) and osteopontin (OPN) were significantly overexpressed in HS arteries. Fisher exact test and annotation-based gene subsets showed that genes upregulated by Jun and Ca 2ϩ /cAMP-response element-binding protein (CREB) were overrepresented. A model of cultured rat cerebrovascular smooth muscle cells was used to test the hypothesis that angiotensin II (ANG II), JunB, and CREB are important in the regulation of genes identified in the rat hypertension model. ANG II induced a transient induction of junB and a delayed induction of PAI-1 and OPN mRNA levels, which were reduced by ERK inhibition with U-0126. Silencing junB using small-interfering RNA reduced mRNA levels of OPN but not PAI-1. The silencing of CREB reduced PAI-1 induction by ANG II but enhanced the transcription of OPN. Together, these results suggest that salt-induced hypertensive disease promotes changes in matricellular genes that are stimulated by ANG II, regulated by ERK, and selectively regulated by JunB and CREB. microarray; Dahl rat; brain arteries; mitogen-activated protein kinase signaling; transcription factors HYPERTENSION IS A multifactorial disease, linked to both genetic and environmental origins, that ultimately causes direct alterations on the vasculature including smooth muscle cell proliferation and vascular remodeling (2, 34, 48). Rats selectively bred for hypertension studies have been useful models to study the complexity of human essential hypertension (42). The Dahl salt-sensitive (Dahl S) genetic model of hypertension is a paradigm of low renin hypertension observed in humans. Two genetic defects have been identified in the Dahl S strain including a mutation of the ␣ 1 Na ϩ , K ϩ -ATPase gene, affecting the renal basolateral epithelia throughout the nephron, and a restriction fragment-length polymorphism in the renin gene, affecting the proximal tubule (19,44).In response to the Na ϩ challenge of a high-...

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JunB Forms the Majority of the AP-1 Complex and Is a Target for Redox Regulation by Receptor Tyrosine Kinase and G Protein-coupled Receptor Agonists in Smooth Muscle Cells

Cited by 107 publications

References 62 publications

Redox factor-1 contributes to the regulation of progression from G₀/G₁ to S by PDGF in vascular smooth muscle cells

Redox factor-1 contributes to the regulation of progression from G₀/G₁ to S by PDGF in vascular smooth muscle cells

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Genes overexpressed in cerebral arteries following salt-induced hypertensive disease are regulated by angiotensin II, JunB, and CREB

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JunB Forms the Majority of the AP-1 Complex and Is a Target for Redox Regulation by Receptor Tyrosine Kinase and G Protein-coupled Receptor Agonists in Smooth Muscle Cells

Cited by 107 publications

References 62 publications

Redox factor-1 contributes to the regulation of progression from G0/G1 to S by PDGF in vascular smooth muscle cells

Redox factor-1 contributes to the regulation of progression from G0/G1 to S by PDGF in vascular smooth muscle cells

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Genes overexpressed in cerebral arteries following salt-induced hypertensive disease are regulated by angiotensin II, JunB, and CREB

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Redox factor-1 contributes to the regulation of progression from G₀/G₁ to S by PDGF in vascular smooth muscle cells

Redox factor-1 contributes to the regulation of progression from G₀/G₁ to S by PDGF in vascular smooth muscle cells