Freeze-Fracture Replica Studies of Tight Junctions in Normal Human Bronchial Epithelium

1989 ◽  
Vol 134 (3) ◽  
pp. 219-226 ◽  
Author(s):  
Hidekatsu Matsumura ◽  
Takao Setoguti
Keyword(s):  
Tight Junctions ◽  
Freeze Fracture ◽  
Bronchial Epithelium ◽  
Normal Human Bronchial Epithelium ◽  
Normal Human

Effect of San-ao Decoction, a traditional Chinese prescription, on IL-4 treated normal human bronchial epithelium

2010 ◽  
Vol 131 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Yu Li ◽  
Ming-Yan Wang ◽  
Xin-sheng Fan ◽  
Xu Qi ◽  
Yan Chen ◽  
...  
Keyword(s):  
Bronchial Epithelium ◽  
Normal Human Bronchial Epithelium ◽  
Normal Human

scholarly journals Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Beata Narożna ◽  
Wojciech Langwiński ◽  
Claire Jackson ◽  
Peter M. Lackie ◽  
John W. Holloway ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profile ◽  
Wound Repair ◽  
Mirna Gene ◽  
Bronchial Epithelium ◽  
Airway Epithelial ◽  
Epithelial Repair ◽  
Mirna Genes ◽  
Normal Human Bronchial Epithelium ◽  
Normal Human

Purpose. Airway epithelium acts as a protective barrier against the particles from the inhaled air. Damage to the epithelium may result in loss of the barrier function. Epithelial repair in response to injury requires complex mechanisms, such as microRNA, small noncoding molecules, to regulate the processes involved in wound repair. We aimed to establish if the microRNA gene expression profile is altered during the airway epithelial repair in differentiated cells. Methods. miRNA gene expression profile during the wound closure of differentiated normal human bronchial epithelium (NHBE) from one donor was analysed using quantitative real-time PCR. We have analysed the expression of 754 genes at five time points during a 48-hour period of epithelium repair using TaqMan Low Density Array. Results. We found out that 233 miRNA genes were expressed in normal human bronchial epithelium. Twenty miRNAs were differentially expressed during the wound repair process, but only one (miR-455-3p) showed significance after FDR adjustment (p=0.02). Using STEM, we have identified two clusters of several miRNA genes with similar expression profile. Pathway enrichment analysis showed several significant signaling pathways altered during repair, mainly involved in cell cycle regulation, proliferation, migration, adhesion, and transcription regulation. Conclusions. miRNA expression profile is altered during airway epithelial repair of differentiated cells from one donor in response to mechanical injury in vitro, suggesting their potential role in wound repair.

Cadherin and catenin expression in normal human bronchial epithelium and non-small cell lung cancer

Lung Cancer ◽  
1999 ◽  
Vol 24 (3) ◽  
pp. 157-168 ◽  
Author(s):  
W.Roy Smythe ◽  
John P. Williams ◽  
Margaret J. Wheelock ◽  
Keith R. Johnson ◽  
Larry R. Kaiser ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Bronchial Epithelium ◽  
Small Cell ◽  
Small Cell Lung ◽  
Normal Human Bronchial Epithelium ◽  
Normal Human

scholarly journals Structural and Functional Regulation of Tight Junctions by RhoA and Rac1 Small GTPases

1998 ◽  
Vol 142 (1) ◽  
pp. 101-115 ◽  
Author(s):  
Tzuu-Shuh Jou ◽  
Eveline E. Schneeberger ◽  
W. James Nelson
Keyword(s):  
Tight Junctions ◽  
Spatial Organization ◽  
Mdck Cells ◽  
Protein Localization ◽  
Freeze Fracture ◽  
Tracer Diffusion ◽  
Small Gtpases ◽  
Dominant Negative ◽  
Solute Diffusion ◽  
Fence Function

Tight junctions (TJ) govern ion and solute diffusion through the paracellular space (gate function), and restrict mixing of membrane proteins and lipids between membrane domains (fence function) of polarized epithelial cells. We examined roles of the RhoA and Rac1 GTPases in regulating TJ structure and function in MDCK cells using the tetracycline repressible transactivator to regulate RhoAV14, RhoAN19, Rac1V12, and Rac1N17 expression. Both constitutively active and dominant negative RhoA or Rac1 perturbed TJ gate function (transepithelial electrical resistance, tracer diffusion) in a dose-dependent and reversible manner. Freeze-fracture EM and immunofluoresence microscopy revealed abnormal TJ strand morphology and protein (occludin, ZO-1) localization in RhoAV14 and Rac1V12 cells. However, TJ strand morphology and protein localization appeared normal in RhoAN19 and Rac1N17 cells. All mutant GTPases disrupted the fence function of the TJ (interdomain diffusion of a fluorescent lipid), but targeting and organization of a membrane protein in the apical membrane were unaffected. Expression levels and protein complexes of occludin and ZO-1 appeared normal in all mutant cells, although ZO-1 was more readily solubilized from RhoAV14-expressing cells with Triton X-100. These results show that RhoA and Rac1 regulate gate and fence functions of the TJ, and play a role in the spatial organization of TJ proteins at the apex of the lateral membrane.

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