title: Epithelium-Specific Ets-Like Transcription Factor 1, ESE-1, Regulates ICAM-1 Expression in Cultured Lung Epithelial Cell Lines.
abstract: Cystic fibrosis (CF) patients suffer from chronic airway inflammation with excessive neutrophil infiltration. Migration of neutrophils to the lung requires chemokine and cytokine signaling as well as cell adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), which plays an important role in mediating adhesive interactions between effector and target cells in the immune system. In this study, we investigated the relationship between ICAM-1 and epithelium-specific ETS-like transcription factor 1 (ESE-1) and found that ICAM-1 expression is upregulated in cell lines of CF (IB3-1) as well as non-CF (BEAS-2B and A549) epithelial origin in response to inflammatory cytokine stimulation. Since ESE-1 is highly expressed in A549 cells without stimulation, we examined the effect of ESE-1 knockdown on ICAM-1 expression in these cells. We found that ICAM-1 expression was downregulated when ESE-1 was knocked down in A549 cells. We also tested the effect of ESE-1 knockdown on cell-cell interactions and demonstrate that the knocking down ESE-1 in A549 cells reduce their interactions with HL-60 cells (human promyelocytic leukemia cell line). These results suggest that ESE-1 may play a role in regulating airway inflammation by regulating ICAM-1 expression.
authors.affiliation: State Key Lab of Respiratory Disease and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510120, China.
authors.forename: Zhiqi
authors.initials: Z
authors.lastname: Yu
authors.affiliation: State Key Lab of Respiratory Disease and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510120, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Xu
authors.affiliation: Protein Modification and Degradation Laboratory, Department of Pathophysiology, Guangzhou Medical University, Guangdong, China.
authors.forename: Jinbao
authors.initials: J
authors.lastname: Liu
authors.affiliation: Physiology & Experimental Medicine Program, Hospital for Sick Children, Toronto, ON, Canada M5G 1X8.
authors.forename: Jing
authors.initials: J
authors.lastname: Wu
authors.affiliation: Physiology & Experimental Medicine Program, Hospital for Sick Children, Toronto, ON, Canada M5G 1X8 ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada M5S 1A8.
authors.forename: Chan Mi
authors.initials: CM
authors.lastname: Lee
authors.affiliation: Department of Pediatrics, Guangzhou First People's Hospital, Affiliated to Guangzhou Medical University, Guangzhou, Guangdong 510180, China.
authors.forename: Li
authors.initials: L
authors.lastname: Yu
authors.affiliation: Physiology & Experimental Medicine Program, Hospital for Sick Children, Toronto, ON, Canada M5G 1X8 ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada M5S 1A8.
authors.forename: Jim
authors.initials: J
authors.lastname: Hu
mesh_terms: D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000235:genetics / Q000502:physiology*; D004847:Epithelial Cells / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D008168:Lung / Q000378:metabolism*; D050783:Proto-Oncogene Proteins c-ets / Q000235:genetics / Q000502:physiology*; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology*
chemical_list: D004268:DNA-Binding Proteins; C105529:ELF3 protein, human; D050783:Proto-Oncogene Proteins c-ets; D014157:Transcription Factors; D018799:Intercellular Adhesion Molecule-1