scholarly journals Genome-wide analysis of HIF-2α chromatin binding sites under normoxia in human bronchial epithelial cells (BEAS-2B) suggests its diverse functions

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Meng-Chang Lee ◽  
Hsin-Ju Huang ◽  
Tzu-Hao Chang ◽  
Hsieh-Chou Huang ◽  
Shen-Yuan Hsieh ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Binding Sites ◽  
Bronchial Epithelial Cells ◽  
Chromatin Binding ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Genome Wide Analysis ◽  
Genome Wide

Interleukin 6-receptor expression on human bronchial epithelial cells: regulation by IL-1 and IL-6

1996 ◽  
Vol 270 (3) ◽  
pp. L346-L352 ◽  
Author(s):  
H. Takizawa ◽  
T. Ohtoshi ◽  
N. Yamashita ◽  
T. Oka ◽  
K. Ito
Keyword(s):  
Epithelial Cells ◽  
Interleukin 6 ◽  
Binding Sites ◽  
Airway Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Receptor Expression ◽  
Airway Epithelial ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Cell Functions

Airway epithelial cells have a potential to participate in regulation of local homeostasis by releasing active compounds including cytokines and growth factors. Several factors such as transforming growth factor-beta and endothelin have been shown to regulate airway epithelial cell functions through an autocrine mechanism. We studied the expression of the specific receptor for a multifunctional cytokine interleukin 6 (IL-6), which is expressed and released by airway epithelial cells. Specific binding assay demonstrated a single set of binding sites on human primary and transformed bronchial epithelial cells. Human interleukin-1alpha (IL-1alpha) increased maximal binding sites to IL-6. Northern blot analysis demonstrated that airway epithelial cells constitutively expressed mRNA for IL-6 receptor (IL-6R), and IL-1alpha and IL-6 itself upregulated IL-6R gene expression. Moreover, exogenously added human recombinant IL-6 had a stimulatory effect on IL-8 release from human bronchial epithelial cells. These results indicated that human bronchial epithelial cells expressed IL-6R, and IL-6 might be involved in the regulation of the epithelial functions via an autocrine as well as a paracrine mechanism.

scholarly journals Genomic signatures of the unjamming transition in compressed human bronchial epithelial cells

2020 ◽  
Author(s):  
Margherita De Marzio ◽  
Ayşe Kılıç ◽  
Enrico Maiorino ◽  
Jennifer Mitchel ◽  
Maureen McGill ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Actin Polymerization ◽  
Bronchial Epithelial Cells ◽  
Epithelial Tissue ◽  
Human Bronchial Epithelial Cells ◽  
Adhesive Interaction ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition ◽  
Genome Wide

AbstractEpithelial tissue has the capacity to switch from a collective phase that is quiescent, solidlike and non-migratory to one that is dynamic, fluid-like and migratory. In certain physiological and pathophysiological contexts this phenotypic switch has been attributed not to the well-known epithelial-to-mesenchymal transition, EMT, but rather to the recently discovered unjamming transition, UJT. UJT has been characterized thus far mainly at functional and morphological levels whereas underlying genome-wide molecular events remain largely unexplored. Using primary human bronchial epithelial cells and one well-defined trigger of UJT –mechanical compression– here we combine temporal RNA-Seq data and Protein-Protein Interaction networks to provide the first genome-wide analysis of UJT. Our results show that compression induces a multiphasic transcriptional response characterized by an early activation of genes regulating the membrane and actomyosin structure, and a delayed activation of genes regulating the extracellular matrix and cellmatrix interactions. This biphasic response is mediated by a cascade of signaling processes that promotes actin polymerization through the recruitment of integrin-ECM adhesive complexes and promotes increased cellular motility through activation of AP-1 transcription factors via ERK and JNK pathways. These findings, taken together, show that the UJT program is not the result of any single signaling pathway but rather comprises a coordinated interplay of downstream pathways including development, fate selection, energy metabolism, cytoskeletal reorganization, and adhesive interaction with extracellular matrix.

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