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

Oliver, Jordan R.; Kushwah, Rahul; Wu, Jing; Pan, Jie; Cutz, Ernest; Yeger, Herman; Waddell, Thomas K.

doi:10.1038/labinvest.2011.100

Cited by 35 publications

(35 citation statements)

References 45 publications

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“…42 In contrast, there was a significantly greater level of cell proliferation and mitosis within the peribronchiolar interstitium of Elf3À/À mice than in wild-type mice. 42 As the absence of Elf3 did not affect the severity of naphthalene-induced Clara cell damage in Elf3À/À mice, 42 the observed differences in airway epithelial repair kinetics between wild-type and Elf3À/À mice were most likely not due to differences in the extent of initial injury. The delayed kinetics of cell proliferation and Clara cell reconstitution observed within the airway epithelium of Elf3À/À mice was more likely due to changes in gene expression for proteins involved in regulating epithelial cell proliferation and/or differentiation during repair after injury.…”

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 89%

“…Indeed, we had also found that Elf3À/À mice express substantially reduced levels of TGF-b RII, which is a well-known transcriptional target gene of Elf3 and is involved in the induction of epithelial cell differentiation, in the bronchiolar airway epithelium both basally and during repair after naphthalene injury. 42 Collectively, these findings suggest that Elf3 plays an important role in the regulation of lung cell proliferation and differentiation during repair of the injured airway epithelium. Furthermore, it is worth noting that as the naphthalene-induced model of acute airway epithelialspecific injury and subsequent repair is not normally associated with excessive inflammation, 43 it is more likely that Elf3 is contributing to this pathophysiological process through its role as a regulator of epithelial homeostasis rather than as a mediator of inflammation.…”

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 92%

“…In similarity to the pathological and physiological processes of lung cancer and lung development, we have recently found an involvement of Elf3 in the regulation of lung regeneration in adult mice after treatment with the Clara cell-specific toxicant, naphthalene. 42 More specifically, the kinetics of cell proliferation and mitosis as well as Clara cell renewal was delayed within the distal bronchiolar airway epithelium of Elf3À/À mice as compared with their wildtype counterparts during repair following naphthaleneinduced Clara cell injury. 42 In contrast, there was a significantly greater level of cell proliferation and mitosis within the peribronchiolar interstitium of Elf3À/À mice than in wild-type mice.…”

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 97%

“…42 More specifically, the kinetics of cell proliferation and mitosis as well as Clara cell renewal was delayed within the distal bronchiolar airway epithelium of Elf3À/À mice as compared with their wildtype counterparts during repair following naphthaleneinduced Clara cell injury. 42 In contrast, there was a significantly greater level of cell proliferation and mitosis within the peribronchiolar interstitium of Elf3À/À mice than in wild-type mice. 42 As the absence of Elf3 did not affect the severity of naphthalene-induced Clara cell damage in Elf3À/À mice, 42 the observed differences in airway epithelial repair kinetics between wild-type and Elf3À/À mice were most likely not due to differences in the extent of initial injury.…”

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 97%

“…34 In human colonic epithelial cells, ESE-1 has also been shown to regulate gene expression of the proinflammatory cytokine, macrophage inflammatory protein-3a (MIP-3a). 39 Another group has previously reported that CR6-interacting factor 1 (Crif1) plays an essential role in Elf3-mediated intestinal development by functioning as a transcriptional co-activator of Elf3 during terminal differentiation of the 25,30 Mouse bronchiolar airway epithelium 42 Mouse embryonal carcinoma cell line (F9) 33,35,37 Human embryonic kidney cell line (HEK 293T) 33,35,37 Human hepatoblastoma cell line (HepG2) 31 Human gastric cancer cell line (SNU-620) 31 Human colon cancer cell line (RKO) 34 Human breast cancer cell lines (SK-BR3, Hs578t) 31,32 Human cervical cancer cell line (HeLa 229) 31,33 Macrophage inflammatory protein-3a (MIP-3a)m Human colonic epithelial cell line (Caco-2) 39 Small proline-rich protein 1B (SPRR1B)m Primary human tracheobronchial epithelial cells 41 Human bronchial epithelial cell line (BEAS-2B) 41 Human lung adenocarcinoma epithelial cell line (NCI-H441) 41 Epithelium-specific ETS transcription factor-3 (ESE-3)m Human bronchial epithelial cell line (BEAS-2B) 44 Human lung carcinoma cell line (A549) 44 Interleukin-6 (IL-6)m Mouse lung tissue 44 Primary mouse airway epithelial cells 47 Primary mouse bone marrow-derived dendritic cells 47 Human bronchial epithelial cell line (BEAS-2B) 47 Interleukin-12 (IL-12)m Primary mouse bone marrow-derived dendritic cells 47 Lysozyme (LYZ)m Primary human bronchial airway epithelial cells 46 Human lung carcinoma cell line (A549) 46 Human lung mucoepidermoid carcinoma-derived cell line (NCI-H292) 46 Human lung adenocarcinoma epithelial cell line (NCI-H441) …”

Section: Ese-1 In Regulating Epithelial Cell Differentiation During Imentioning

confidence: 99%

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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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Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 89%

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 92%

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 97%

Section: Ese-1 In Lung Cancer Development and Regenerationmentioning

confidence: 97%

Section: Ese-1 In Regulating Epithelial Cell Differentiation During Imentioning

confidence: 99%

See 3 more Smart Citations

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

Oliver

Kushwah

2012

Laboratory Investigation

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ESE1/AGR2 axis antagonizes TGF‐β‐induced epithelial‐mesenchymal transition in low‐grade pancreatic cancer

Bai

Tian

et al. 2022

Cancer Medicine

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Airway epithelial cell differentiation during lung organogenesis requires C/EBPα and C/EBPβ

Roos

Berg

Barton

et al. 2012

Developmental Dynamics

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Background: CCAAT/enhancer‐binding protein (C/EBP)α is crucial for lung development and differentiation of the pulmonary epithelium. Conversely, no lung defects have been observed in C/EBPβ‐deficient mice, although C/EBPβ trans‐activate pulmonary genes by binding to virtually identical DNA‐sequences as C/EBPα. Thus, the pulmonary phenotype of mice lacking C/EBPβ could be explained by functional replacement with C/EBPα. We investigated whether C/EBPα and C/EBPβ have overlapping functions in regulating lung epithelial differentiation during organogenesis. Epithelial differentiation was assessed in mice with a lung epithelial–specific (SFTPC‐Cre‐mediated) deletion of C/EBPα (CebpaΔLE), C/EBPβ (CebpbΔLE), or both genes (CebpaΔLE; CebpbΔLE). Results: Both CebpaΔLE mice and CebpaΔLE; CebpbΔLE mice demonstrated severe pulmonary immaturity compared to wild‐type littermates, while no differences in lung histology or epithelial differentiation were observed in CebpbΔLE mice. In contrast to CebpaΔLE mice, CebpaΔLE; CebpbΔLE mice also displayed undifferentiated Clara cells with markedly impaired protein and mRNA expression of Clara cell secretory protein (SCGB1A1), compared to wild‐type littermates. In addition, ectopic mucus‐producing cells were observed in the conducting airways of CebpaΔLE; CebpbΔLE mice. Conclusions: Our findings demonstrate that C/EBPα and C/EBPβ play pivotal, and partly overlapping roles in determining airway epithelial differentiation, with possible implications for tissue regeneration in lung homeostasis and disease. Developmental Dynamics 241:911–923, 2012. © 2012 Wiley Periodicals, Inc.

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

Cited by 35 publications

References 45 publications

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

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

ESE1/AGR2 axis antagonizes TGF‐β‐induced epithelial‐mesenchymal transition in low‐grade pancreatic cancer

Airway epithelial cell differentiation during lung organogenesis requires C/EBPα and C/EBPβ

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