scholarly journals Stimulus-dependent dissociation between XB130 and Tks5 scaffold proteins promotes airway epithelial cell migration

Oncotarget ◽  
2016 ◽  
Vol 7 (47) ◽  
pp. 76437-76452 ◽  
Author(s):  
Serisha Moodley ◽  
Mathieu Derouet ◽  
Xiao Hui Bai ◽  
Feng Xu ◽  
Andras Kapus ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Airway Epithelial Cell ◽  
Scaffold Proteins ◽  
Airway Epithelial ◽  
Epithelial Cell Migration

Effects of corticosteroid-induced apoptosis on airway epithelial wound closure in vitro

2006 ◽  
Vol 291 (4) ◽  
pp. L794-L801 ◽  
Author(s):  
Delbert R. Dorscheid ◽  
Benjamin J. Patchell ◽  
Oscar Estrada ◽  
Bertha Marroquin ◽  
Roberta Tse ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Untreated Control ◽  
Wound Closure ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Wound Area ◽  
Epithelial Cell Migration

Damage to the airway epithelium is common in asthma. Corticosteroids induce apoptosis in and suppress proliferation of airway epithelial cells in culture. Whether apoptosis contributes to impaired epithelial cell repair after injury is not known. We examined whether corticosteroids would impair epithelial cell migration in an in vitro model of wound closure. Wounds (∼0.5–1.3 mm2) were created in cultured 1HAEo−human airway epithelial cell monolayers, after which cells were treated with up to 10 μM dexamethasone or budesonide for 24 h. Cultured cells were pretreated for 24 or 48 h with dexamethasone to observe the effect of long-term exposure on wound closure. After 12 h, the remaining wound area in monolayers pretreated for 48 h with 10 μM dexamethasone was 43 ± 18% vs. 10 ± 8% for untreated control monolayers. The addition of either corticosteroid immediately after injury did not slow closure significantly. After 12 h the remaining wound area in monolayers treated with 10 μM budesonide was 39 ± 4% vs. 43 ± 3% for untreated control monolayers. The proportion of apoptotic epithelial cells as measured by terminal deoxynucleotidyltransferase-mediated dUTP biotin nick end labeling both at and away from the wound edge was higher in monolayers treated with budesonide compared with controls. However, wound closure in the apoptosis-resistant 1HAEo−.Bcl-2+cell line was not different after dexamethasone treatment. We demonstrate that corticosteroid treatment before mechanical wounding impairs airway epithelial cell migration. The addition of corticosteroids after injury does not slow migration, despite their ability to induce apoptosis in these cells.

scholarly journals p120-Catenin modulates airway epithelial cell migration induced by cigarette smoke

2012 ◽  
Vol 417 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Lili Zhang ◽  
Marianne Gallup ◽  
Lorna Zlock ◽  
Walter Finkbeiner ◽  
Nancy A. McNamara
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Cigarette Smoke ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
P120 Catenin ◽  
Epithelial Cell Migration

scholarly journals Airway Epithelial Cell Migration and Wound Repair by ATP-mediated Activation of Dual Oxidase 1

2006 ◽  
Vol 282 (5) ◽  
pp. 3213-3220 ◽  
Author(s):  
Umadevi V. Wesley ◽  
Peter F. Bove ◽  
Milena Hristova ◽  
Sean McCarthy ◽  
Albert van der Vliet
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Wound Repair ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Epithelial Cell Migration ◽  
Dual Oxidase

scholarly journals Dual Oxidase–1 Is Required for Airway Epithelial Cell Migration and Bronchiolar Reepithelialization after Injury

2013 ◽  
Vol 48 (3) ◽  
pp. 337-345 ◽  
Author(s):  
Stefan H. Gorissen ◽  
Milena Hristova ◽  
Aida Habibovic ◽  
Lynne M. Sipsey ◽  
Page C. Spiess ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Epithelial Cell Migration ◽  
Dual Oxidase

scholarly journals Fibronectin matrix polymerization regulates small airway epithelial cell migration

2003 ◽  
Vol 285 (1) ◽  
pp. L169-L179 ◽  
Author(s):  
Denise C. Hocking ◽  
Cecilia H. Chang
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Epithelial Cell ◽  
Cell Motility ◽  
Airway Epithelial Cell ◽  
Small Airway ◽  
Airway Epithelial ◽  
Small Airway Epithelial Cell ◽  
Fibronectin Matrix ◽  
Matrix Polymerization

The continuous conversion of soluble fibronectin into extracellular matrix fibrils occurs through a dynamic, cell-dependent process. As the extracellular matrix is assembled, changes in the conformation of matrix proteins may expose biologically active, matricryptic sites that alter cell behavior. In this study, an in vitro model of wound healing was used to determine the role of matrix fibronectin in airway epithelial cell motility. Our findings indicate that, under basal conditions, small airway epithelial cell (SAEC) migration requires active fibronectin matrix polymerization. Furthermore, SAEC migration is increased significantly by the interaction of cells with a recombinant construct containing fibronectin's matricryptic III-1 site. In contrast, addition of increasing amounts of fibronectin to SAECs significantly decreased the rate of cell migration. This fibronectin-induced inhibition of cell migration was overcome by blocking excess fibronectin matrix deposition. These data indicate that SAEC migration is regulated in a biphasic manner by the polymerization of fibronectin in the extracellular matrix and suggest a stimulatory role for fibronectin's matricryptic III-1 site in cell motility.

Role of cell surface glycosylation in mediating repair of human airway epithelial cell monolayers

2001 ◽  
Vol 281 (4) ◽  
pp. L982-L992 ◽  
Author(s):  
Delbert R. Dorscheid ◽  
Kimberly R. Wojcik ◽  
Kelly Yule ◽  
Steven R. White
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Epithelial Cell ◽  
Cell Surface ◽  
Functional Role ◽  
Wound Repair ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Epidermal Growth

Our laboratory recently demonstrated the pattern of cell surface glycosylation of nonsecretory central airway epithelium (Dorscheid DR, Conforti AE, Hamann KJ, Rabe KF, and White SR. Histochem J 31: 145–151, 1999), but the role of glycosylation in airway epithelial cell migration and repair is unknown. We examined the functional role of cell surface carbohydrates in wound repair after mechanical injury of 1HAEo− human airway epithelial and primary bronchial epithelial monolayers. Wound repair stimulated by epidermal growth factor was substantially attenuated by 10−7 M tunicamycin (TM), an N-glycosylation inhibitor, but not by the inhibitors deoxymannojirimycin or castanospermine. Wound repair of 1HAEo− and primary airway epithelial cells was blocked completely by removal of cell surface terminal fucose residues by α-fucosidase. Cell adhesion to collagen matrix was prevented by TM but was only reduced ∼20% from control values with prior α-fucosidase treatment. Cell migration in Blind Well chambers stimulated by epidermal growth factor was blocked by pretreatment with TM but α-fucosidase pretreatment produced no difference from control values. These data suggest that cell surface N-glycosylation has a functional role in airway epithelial cell adhesion and migration and that N-glycosylation with terminal fucosylation plays a role in the complex process of repair by coordination of certain cell-cell functions.

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