cAMP-Response Element-Binding Protein Mediates Tumor Necrosis Factor-α–Induced Vascular Smooth Muscle Cell Migration

Ono, Hiroki; Ichiki, Toshihiro; Fukuyama, Kae; Iino, Naoko; Masuda, Shinya; Egashira, Kensuke; Takeshita, Akira

doi:10.1161/01.atv.0000138052.86051.0d

Cited by 45 publications

(47 citation statements)

References 46 publications

(40 reference statements)

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“…These findings clearly suggest that AA-induced VSMC motility requires the activation of all three major groups of MAPKs. One recent study reported that CREB-1 plays a role in tumor necrosis factor-a-induced VSMC motility (34). In addition, other studies have reported that MAPKs, particularly ERKs, JNKs, and p38MAPK, via phosphorylating serine-133, modulate CREB-1 activity (26, 27, 29).…”

Section: Creb-1 Mediates Arachidonic Acid-induced Vsmc Motilitymentioning

confidence: 99%

“…Vascular smooth muscle cell (VSMC) migration and proliferation are major contributing factors in the pathogenesis of vascular inflammatory diseases such as atherosclerosis and restenosis (18). Studies from several laboratories, including ours, have revealed the involvement of the ATF/CREB family of transcriptional factors in both the positive and negative regulation of VSMC growth and motility (30)(31)(32)(33)(34)(35)(36). To determine whether AA is a chemoattractant for VSMC and, if it is, what the underlying mechanisms are, we studied the effects of AA and the role of CREB-1 in VSMC motility.…”

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confidence: 96%

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Involvement of cAMP-response element binding protein-1 in arachidonic acid-induced vascular smooth muscle cell motility

Dronadula

Rizvi

Blaskova

et al. 2006

Journal of Lipid Research

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In addition to their role in many vital cellular functions, arachidonic acid (AA) and its eicosanoid metabolites are involved in the pathogenesis of several diseases, including atherosclerosis and cancer. To understand the potential mechanisms by which these lipid molecules could influence the disease processes, particularly cardiovascular diseases, we studied AA's effects on vascular smooth muscle cell (VSMC) motility and the role of cAMPresponse element binding protein-1 (CREB-1) in this process. AA exerted differential effects on VSMC motility; at lower doses, it stimulated motility, whereas at higher doses, it was inhibitory. AA-induced VSMC motility requires its conversion via the lipoxygenase (LOX) and cyclooxygenase (COX) pathways. AA stimulated the phosphorylation of extracellular signal-regulated kinases (ERKs), Jun N-terminal kinases ( JNKs), and p38 mitogen-activated protein kinase (p38MAPK) in a time-dependent manner, and blockade of these serine/threonine kinases significantly attenuated AAinduced VSMC motility. In addition, AA stimulated CREB-1 phosphorylation and activity in a manner that was also dependent on its metabolic conversion via the LOX and COX pathways and the activation of ERKs and p38MAPK but not JNKs. Furthermore, suppression of CREB-1 activation inhibited AA-induced VSMC motility. 15(S)-Hydroxyeicosatetraenoic acid and prostaglandin F 2a , the 15-LOX and COX metabolites of AA, respectively, that are produced by VSMC at lower doses, were also found to stimulate motility in these cells. Together, these results suggest that AA induces VSMC motility by complex mechanisms involving its metabolism via the LOX and COX pathways as well as the ERK-and p38MAPK-dependent and JNK-independent activation of CREB-1.-Dronadula, N., F. Rizvi, E. Blaskova, Q. Li, and G. N. Rao. Involvement of cAMP-response element binding protein-1 in arachidonic acid-induced vascular smooth muscle cell motility. J. Lipid Res. 2006. 47: 767-777.

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Section: Creb-1 Mediates Arachidonic Acid-induced Vsmc Motilitymentioning

confidence: 99%

mentioning

confidence: 96%

Involvement of cAMP-response element binding protein-1 in arachidonic acid-induced vascular smooth muscle cell motility

Dronadula

Rizvi

Blaskova

et al. 2006

Journal of Lipid Research

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“…Cyclic AMPincreasing agents have been shown to regulate cell migration (Howe, 2004;Howe et al, 2005) and to exert the inhibitory effect through cAMP-dependent protein kinase A (PKA) in fibroblasts (Kohyama et al, 2001) and through cAMP response element-binding protein in vascular smooth muscle cells (Ono et al, 2004). However, there are increasThis article was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E09 -08 -0692) on October 28, 2009.…”

Section: Introductionmentioning

confidence: 99%

“…Cyclic AMPincreasing agents have been shown to regulate cell migration (Howe, 2004;Howe et al, 2005) and to exert the inhibitory effect through cAMP-dependent protein kinase A (PKA) in fibroblasts (Kohyama et al, 2001) and through cAMP response element-binding protein in vascular smooth muscle cells (Ono et al, 2004). However, there are increas-ing numbers of reports showing that cAMP can also activate small GTPase Rap1 through stimulating Epac, an exchange protein directly activated by cAMP (de Rooij et al, 1998;Kawasaki et al, 1998;Enserink et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Role of Rap1B and Tumor Suppressor PTEN in the Negative Regulation of Lysophosphatidic Acid—induced Migration by Isoproterenol in Glioma Cells

Malchinkhuu

Sato

Maehama

et al. 2009

MBoC

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The clarification of mechanisms that negatively regulate the invasive behavior of human glioma cells is of great importance in order to find new methods of treatment. In this study, we have focused on the negative regulation of lysophosphatidic acid (LPA)-induced migration in glioma cells. Using small interference RNA and dominant-negative gene strategies in addition to pharmacological tools, we found that isoproterenol (ISO) and sphingosine-1-phosphate (S1P) negatively but differently regulate the LPA-induced migration. ISO-induced suppression of the migration of glioma cells occurs via ␤ 2 -adrenergic receptor/cAMP/Epac/Rap1B/inhibition of Rac, whereas S1P has been shown to suppress the migration of the cells through S1P 2 receptor/Rho-mediated down-regulation of Rac1. The expression of tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is required for the inhibitory ISO-induced and Rap1B-mediated actions on the migration, Rac1 activation, and Akt activation in response to LPA. Thus, the PTENmediated down-regulation of phosphatidylinositol 3-kinase activity may be involved in the regulation of Rap1B-dependent inhibition of Rac1 activity. These findings suggest that there are at least two distinct inhibitory pathways, which are mediated by the S1P 2 receptor and ␤ 2 -adrenergic receptor, to control the migratory, hence invasive, behavior of glioma cells. INTRODUCTIONThe malignant astrocytomas, the anaplastic astrocytoma and glioblastoma multiforme, are the most common glial tumors, with an annual incidence of three to four per 100,000 of population (DeAngelis, 2001). Because radical surgical treatment of malignant glial tumors is impossible because of the highly expressed migratory and invasive features of glioma cells, further understanding of the complex regulation and signaling molecules involved in glioma invasion is still needed. Lysophosphatidic acid (LPA) has been shown to play a significant role in human tumorigenesis as a factor to increase the motility and invasiveness of different cell types (Imamura et al., 1993;Stam et al., 1998). In glioma cells as well, extracellularly added LPA induced the proliferation and migration of stimulated cells (Malchinkhuu et al., 2005). A major part of extracellular LPA is thought to be produced from lysophosphatidylcholine by autotaxin/lysophospholipase D (Tokumura et al., 2002;Umezu-Goto et al., 2002). In the CNS as well, LPA production seems to occur in a similar way . Recent evidence suggested that autotaxin is overexpressed in glioblastoma multiforme and contributes to the cell motility of glioblastomas (Kishi et al., 2006). For this reason, revealing new substances or mechanisms that could negatively regulate the LPA-induced invasive behavior is of great importance for devising new and effective treatment modalities to counteract tumor cells.Our previous studies (Malchinkhuu et al., 2005(Malchinkhuu et al., , 2008 and those from other laboratories (Lepley et al., 2005) suggest that sphingosine 1-phosphate (S1P) and its receptors are ...

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“…ATF5, encoded by ATF5 gene, belongs to the ATF/cyclic adenosine monophosphate response-element binding (CREB) protein family (40). CREB has been reported to serve a role in modulating the apoptosis and proliferation of vascular smooth muscle cells (41,42).…”

Section: Discussionmentioning

confidence: 99%

A comprehensive analysis of differentially expressed genes and pathways in abdominal aortic aneurysm

Yuan

Liang

Zhang

2015

Molecular Medicine Reports

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Abstract. The current study aimed to investigate the molecular mechanism underlying abdominal aortic aneurysm (AAA) via various bioinformatics techniques. Gene expression profiling analysis of differentially expressed genes (DEGs) between AAA samples and normal controls was conducted. The Database for Annotation, Visualization and Integrated Discovery tool was utilized to perform Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses for DEGs and clusters from the protein-protein interaction (PPI) network, which was constructed using the Search Tool for the Retrieval of Interacting Genes. In addition, important transcription factors (TFs) that regulated DEGs were investigated. A total of 346 DEGs were identified between AAA samples and healthy controls. Additionally, four clusters were identified from the PPI network. Cluster 1 was associated with sensory perception of smell and the olfactory transduction subpathway. The most significant GO function terms for cluster 2 and 3 were response to virus and defense response, respectively. Cluster 4 was associated with mitochondria-associated functions and the oxidative phosphorylation subpathway. Early growth response-1 (EGR-1), Myc, activating transcription factor 5 (ATF5) and specificity protein (SP) 1:SP3 were identified to be critical TFs in this disease. The present study suggested that the olfactory transduction subpathway, mitochondria and oxidative phosphorylation pathways were involved in AAA, and TFs, such as EGR-1, Myc, ATF5 and SP1:SP3, may be potential candidate molecular targets for this disease.

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cAMP-Response Element-Binding Protein Mediates Tumor Necrosis Factor-α–Induced Vascular Smooth Muscle Cell Migration

Cited by 45 publications

References 46 publications

Involvement of cAMP-response element binding protein-1 in arachidonic acid-induced vascular smooth muscle cell motility

Involvement of cAMP-response element binding protein-1 in arachidonic acid-induced vascular smooth muscle cell motility

Role of Rap1B and Tumor Suppressor PTEN in the Negative Regulation of Lysophosphatidic Acid—induced Migration by Isoproterenol in Glioma Cells

A comprehensive analysis of differentially expressed genes and pathways in abdominal aortic aneurysm

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