ESE-1 Is a Novel Transcriptional Mediator of Inflammation That Interacts with NF-κB to Regulate the Inducible Nitric-oxide Synthase Gene

Rudders, Susan A.; Gaspar, John; Madore, Rebecca; Voland, Carole; Grall, Franck; Patel, Anand; Pellacani, Andrea; Perrella, Mark A.; Libermann, Towia A.; Oettgen, Peter

doi:10.1074/jbc.m006507200

Cited by 94 publications

(137 citation statements)

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“…Although the expression of ESEs is normally confined to epithelial cells, cytokineregulated ESE expression exists in other cell types. For example, in response to inflammatory cytokines, ESE-1 is expressed in monocytes [23], chondrocytes and fibroblasts [24,25]. We report here that the expression of ESE-1 and ESE-3 in airway epithelial cells can be dramatically enhanced by inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 72%

“…To examine whether ESE-1 and ESE-3 expression in epithelial cells can be induced by IL-1β and/or TNF-α as in non-epithelial cells [23][24][25][26], we stimulated cultured human bronchial epithelial cells (BEAS-2B) with IL-1β and/or TNF-α. Using semi-quantitative RT-PCR (data not shown), we detected increased ESE-1 and ESE-3 but not ESE-2 mRNA expression after cytokine induction.…”

Section: Ese-1 and Ese-3 Are Upregulated In Bronchial Epithelial Cellmentioning

confidence: 99%

“…The expression of ESE-1 can be induced by inflammatory cytokines (IL-1β and TNF-α) in cultured non-epithelial cells, such as vascular smooth muscle cells, endothelial cells, monocytes [23] and fibroblasts [24,25]. ESE-3 mRNA expression is induced in bronchial smooth muscle cells and fibroblasts and is constitutively expressed in human bronchial epithelial cells [26].…”

Section: Introductionmentioning

confidence: 99%

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Regulation of epithelium-specific Ets-like factors ESE-1 and ESE-3 in airway epithelial cells: potential roles in airway inflammation

Duan

Cao

et al. 2008

Cell Res

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Airway inflammation is the hallmark of many respiratory disorders, such as asthma and cystic fibrosis. Changes in airway gene expression triggered by inflammation play a key role in the pathogenesis of these diseases. Genetic linkage studies suggest that ESE-2 and ESE-3, which encode epithelium-specific Ets-domain-containing transcription factors, are candidate asthma susceptibility genes. We report here that the expression of another member of the Ets family transcription factors ESE-1, as well as ESE-3, is upregulated by the inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in bronchial epithelial cell lines. Treatment of these cells with IL-1β and TNF-α resulted in a dramatic increase in mRNA expression for both ESE-1 and ESE-3. We demonstrate that the induced expression is mediated by activation of the transcription factor NF-κB. We have characterized the ESE-1 and ESE-3 promoters and have identified the NF-κB binding sequences that are required for the cytokine-induced expression. In addition, we also demonstrate that ESE-1 upregulates ESE-3 expression and downregulates its own induction by cytokines. Finally, we have shown that in Elf3 (homologous to human ESE-1) knockout mice, the expression of the inflammatory cytokine interleukin-6 (IL-6) is downregulated. Our findings suggest that ESE-1 and ESE-3 play an important role in airway inflammation.

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Section: Discussionmentioning

confidence: 72%

Section: Ese-1 and Ese-3 Are Upregulated In Bronchial Epithelial Cellmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of epithelium-specific Ets-like factors ESE-1 and ESE-3 in airway epithelial cells: potential roles in airway inflammation

Duan

Cao

et al. 2008

Cell Res

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“…41 Interestingly, it has been shown that induction of SPRR1B gene expression in bronchial epithelial cells is mediated in part by protein-protein interactions between ESE-1 and other transcription factors, such as specificity protein 1 and activator protein 1 (AP-1), at the proximal and distal promoter regions, respectively. 41 With regards to lung development, very high levels of Elf3 expression have previously been detected within the Primary human aortic smooth muscle cells (HASMCs) 69,72 Primary rat aortic smooth muscle cells (RASMCs) 69,72 Human acute monocytic leukemia cell line (THP-1) 69 Mouse leukaemic monocyte macrophage cell line (RAW 264.7) 69 Mouse thoracic aorta smooth muscle and endothelium ESE-1 in development and disease JR Oliver et al developing fetal mouse lung. 16 However, further experiments are definitely required to obtain a better understanding of the exact role played by this transcription factor in both lung cancer and development.…”

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 99%

Multiple roles of the epithelium-specific ETS transcription factor, ESE-1, in development and disease

Oliver

Kushwah

2012

Laboratory Investigation

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The E26 transformation-specific (ETS) family of transcription factors comprises of 27 and 26 members in humans and mice, respectively, which are known to regulate many different biological processes, including cell proliferation, cell differentiation, embryonic development, neoplasia, hematopoiesis, angiogenesis, and inflammation. The epitheliumspecific ETS transcription factor-1 (ESE-1) is a physiologically important ETS transcription factor, which has been shown to play a role in the pathogenesis of various diseases, and was originally characterized as having an epithelial-restricted expression pattern, thus placing it within the epithelium-specific ETS subfamily. Despite a large body of published work on ETS biology, much remains to be learned about the precise functions of ESE-1 and other epithelium-specific ETS factors in regulating diverse disease processes. Clues as to the specific function of ESE-1 in the setting of various diseases can be obtained from studies aimed at examining the expression of putative target genes regulated by ESE-1. Thus, this review will focus primarily on the various roles of ESE-1 in different pathophysiological processes, including regulation of epithelial cell differentiation during both intestinal development and lung regeneration; regulation of dendritic cell-driven T-cell differentiation during allergic airway inflammation; regulation of mammary gland development and breast cancer; and regulation of the effects of inflammatory stimuli within the setting of synovial joint and vascular inflammation. Understanding the exact mechanisms by which ESE-1 regulates these processes can have important implications for the treatment of a wide range of diseases. KEYWORDS: cancer; development; epithelial cell differentiation; ESE-1; ETS transcription factor; inflammation; regeneration The E26 transformation-specific (ETS) family of transcription factors is characterized by a highly conserved 84-aminoacid DNA-binding domain, known as the ETS domain. 1 Because the first member of the ETS family, the v-ets oncogene, was originally discovered as part of a fusion protein with gag and myb expressed by the E26 avian erythroblastosis-transforming retrovirus and its DNA-binding domain is E26 transformation-specific, this 84-amino-acid DNA-binding domain was named the ETS domain. 1 The ETS domain is usually located within the carboxyl-terminal region of the protein as a winged helix-turn-helix structural motif and mediates binding to sites of purine-rich DNA, commonly containing a core consensus sequence of GGAA/T, within the promoter and enhancer regions of target genes. 2,3 Many ETS transcription factors also contain a pointed domain, which is located within the amino-terminal region and is involved in protein-protein interactions. 2 Approximately 30 members of the ETS transcription factor family have been identified in mammals (ie 27 in humans and 26 in mice), 4 and have been shown to play crucial roles in the regulation of many physiological and pathological processes, such as embryonic develo...

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“…22,23 It is also worthy to note that although Elf3 is believed to be expressed exclusively in epithelial cells, this may only be the case under basal conditions as previous studies have shown that expression of human ESE-1 can be induced by proinflammatory cytokines in nonepithelial cells, such as synovial fibroblasts, chondrocytes, osteoblasts, monocytes/macrophages, vascular smooth muscle cells, and endothelial cells. 24,25 Interestingly, expression of human ESE-1 was also shown to occur in some lung cancers, such as large cell carcinoma and adenocarcinoma, and in lung cancer-derived cell lines, such as A549. 22 In addition, even though low levels of Elf3 expression were detected in adult mouse lung, very high levels of expression were reported in developing fetal mouse lung.…”

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confidence: 99%

Elf3 plays a role in regulating bronchiolar epithelial repair kinetics following Clara cell-specific injury

Oliver

Kushwah

et al. 2011

Laboratory Investigation

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ESE-1 Is a Novel Transcriptional Mediator of Inflammation That Interacts with NF-κB to Regulate the Inducible Nitric-oxide Synthase Gene

Cited by 94 publications

References 53 publications

Regulation of epithelium-specific Ets-like factors ESE-1 and ESE-3 in airway epithelial cells: potential roles in airway inflammation

Regulation of epithelium-specific Ets-like factors ESE-1 and ESE-3 in airway epithelial cells: potential roles in airway inflammation

Multiple roles of the epithelium-specific ETS transcription factor, ESE-1, in development and disease

Elf3 plays a role in regulating bronchiolar epithelial repair kinetics following Clara cell-specific injury

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