TNFα induces expression of transcription factors c-fos, Egr-1, and Ets-1 in vascular lesions through extracellular signal-regulated kinases 1/2

Goetze, Stephan; Kintscher, Ulrich; Kaneshiro, Kristina; Meehan, Woerner P.; Collins, Alan R.; Fleck, Eckart; Hsueh, Willa A.; Law, Ronald E.

doi:10.1016/s0021-9150(01)00497-x

Cited by 124 publications

(83 citation statements)

References 51 publications

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“…For example, the TNF-␣ gene is regulated by ETS-1 (24). TNF-␣ can also induce the expression of ETS-1 and is up-regulated in animal models of vascular inflammation (40). ETS-1 has also been shown to be enriched in angiogenic blood vessels and can cooperate with another transcription factor, HIF-1␣, to regulate the expression of the VEGF receptor Flk-1 (41,42).…”

Section: Discussionmentioning

confidence: 99%

ESE-1 Is a Novel Transcriptional Mediator of Angiopoietin-1 Expression in the Setting of Inflammation

Brown

Gaspar

Pettit

et al. 2004

Journal of Biological Chemistry

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Angiogenesis is a critical component of the inflammatory response associated with a number of conditions. Angiopoietin-1 (Ang-1) is an angiogenic growth factor that promotes the chemotaxis of endothelial cells and facilitates the maturation of new blood vessels. Ang-1 expression is up-regulated in response to tumor necrosis factor-␣ (TNF-␣). To begin to elucidate the underlying molecular mechanisms by which Ang-1 gene expression is regulated during inflammation, we isolated 3.

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Section: Discussionmentioning

confidence: 99%

ESE-1 Is a Novel Transcriptional Mediator of Angiopoietin-1 Expression in the Setting of Inflammation

Brown

Gaspar

Pettit

et al. 2004

Journal of Biological Chemistry

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“…The c-Fos gene is also known to regulate the growth, differentiation, and migration of a variety of vascular and non-vascular cells, and to regulate matrix degradation [18]. A panel of genes, including c-Fos, that were differentially expressed in microarray analysis, was clearly able to identify acute ischemic stroke patients from healthy subjects [19].…”

Section: C-fos and Atherosclerosismentioning

confidence: 99%

Smoking and FOS expression from blood leukocyte transcripts in patients with coronary artery disease

et al. 2011

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“…Other proinflammatory cytokines have also been reported to mediate a potent immune response after vasculature injury that involves ERK1/2. For example, TNF-α initiates an ERK1/2-dependent expression of several transcription factors in VSM cells in a vascular injury model [48] and has also been shown to stimulate the expression of iNOS in an ERK1/2-dependent manner in cultured VSM cells [35].…”

Section: The Role Of Map Kinase and Protein Kinase C In Regulating Inmentioning

confidence: 99%

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

Ginnan

Guikema

Halligan

et al. 2008

Free Radical Biology and Medicine

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Inflammation plays a critical role in promoting smooth muscle migration and proliferation during vascular diseases such as post-angioplasty restenosis and atherosclerosis. Another common feature of many vascular diseases is the contribution of reactive oxygen (ROS) and nitrogen (RNS) species to vascular injury. Primary sources of ROS and RNS in smooth muscle are several isoforms of NADPH oxidase (Nox) and the cytokine-regulated inducible nitric oxide (NO) synthase (iNOS). One important example of the interaction between NO and ROS is the reaction of NO with superoxide to yield peroxynitrite, which may contribute to the pathogenesis of hypertension. In this review, we discuss the literature that supports an alternate possibility: Nox-derived ROS modulate NO bioavailability by altering the expression of iNOS. We highlight data showing co-expression of iNOS and Nox in vascular smooth muscle and demonstrating the functional consequences of iNOS and Nox during vascular injury. We describe the relevant literature demonstrating that the mitogen activated protein kinases (MAP kinases) are important modulators of pro-inflammatory cytokinedependent expression of iNOS. A central hypothesis discussed is that ROS-dependent regulation of the serine/threonine kinase protein kinase Cδ (PKCδ) is essential to understanding how Nox may regulate signaling pathways leading to iNOS expression. Overall, the integration of non-phagocytic NADPHoxidase with cytokine signaling in general and in vascular smooth muscle in particular is poorly understood and merit further investigation.

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TNFα induces expression of transcription factors c-fos, Egr-1, and Ets-1 in vascular lesions through extracellular signal-regulated kinases 1/2

Cited by 124 publications

References 51 publications

ESE-1 Is a Novel Transcriptional Mediator of Angiopoietin-1 Expression in the Setting of Inflammation

ESE-1 Is a Novel Transcriptional Mediator of Angiopoietin-1 Expression in the Setting of Inflammation

Smoking and FOS expression from blood leukocyte transcripts in patients with coronary artery disease

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

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