Changes in basal cell subpopulations and tissue differentiation in human epidermal cultures treated with epidermal growth factor and cholera toxin

1985 ◽  
Vol 49 (1) ◽  
pp. 325-340 ◽  
Author(s):  
P. K. A. Jensen ◽  
J. O. R. Nørgård ◽  
L. Bolund
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cholera Toxin ◽  
Basal Cell ◽  
Tissue Differentiation ◽  
Epidermal Growth ◽  
Cell Subpopulations

Epidermal Growth Factor Up-Regulates Sodium-Glucose Cotransport in Enterocyte Models in the Presence of Cholera Toxin

1997 ◽  
Vol 21 (4) ◽  
pp. 185-191 ◽  
Author(s):  
Devendra I. Mehta ◽  
Karoly Horváth ◽  
Somchoke Chanasongcram ◽  
Ivor D. Hill ◽  
Pinaki Panigrahi
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cholera Toxin ◽  
Epidermal Growth ◽  
Sodium Glucose Cotransport

The B subunit of cholera toxin enhances DNA synthesis in rat hepatocytes induced by insulin and epidermal growth factor

1991 ◽  
Vol 174 (1) ◽  
pp. 372-378 ◽  
Author(s):  
Hiroshi Mitsui ◽  
Masao Iwamori ◽  
Naoaki Hashimoto ◽  
Haruki Yamada ◽  
Yusei Ikeda ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Cholera Toxin ◽  
Rat Hepatocytes ◽  
B Subunit ◽  
Epidermal Growth

scholarly journals Epidermal growth factor receptor activity is necessary for mouse basal cell proliferation

2014 ◽  
Vol 307 (10) ◽  
pp. L800-L810 ◽  
Author(s):  
Heather M. Brechbuhl ◽  
Bilan Li ◽  
Russell W. Smith ◽  
Susan D. Reynolds
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Basal Cell ◽  
Basal Cells ◽  
Epithelial Repair ◽  
Epidermal Growth ◽  
Proliferation In Vitro

ERB family receptors (EGFR, ERB-B2, ERB-B3, and ERB-B4) regulate epithelial cell function in many tissue types. In the human airway epithelium, changes in ERB receptor expression are associated with epithelial repair defects. However, the specific role(s) played by ERB receptors in repair have not been determined. We aimed to determine whether ERB receptors regulate proliferation of the tracheobronchial progenitor, the basal cell. Receptor tyrosine kinase arrays were used to evaluate ERB activity in normal and naphthalene (NA)-injured mouse trachea and in air-liquid interface cultures. Roles for epidermal growth factor (EGF), EGFR, and ERB-B2 in basal cell proliferation were evaluated in vitro. NA injury and transgenic expression of an EGFR-dominant negative (DN) receptor were used to evaluate roles for EGFR signaling in vivo. EGFR and ERB-B2 were active in normal and NA-injured trachea and were the only active ERB receptors detected in proliferating basal cells in vitro. EGF was necessary for basal cell proliferation in vitro. The EGFR inhibitor, AG1478, decreased proliferation by 99, and the Erb-B2 inhibitor, AG825, decreased proliferation by ∼66%. In vivo, EGFR-DN expression in basal cells significantly decreased basal cell proliferation after NA injury. EGF and EGFR are necessary for basal cell proliferation. The EGFR/EGFR homo- and the EGFR/ERB-B2 heterodimer account for ∼34 and 66%, respectively, of basal cell proliferation in vitro. Active EGFR is necessary for basal cell proliferation after NA injury. We conclude that EGFR activation is necessary for mouse basal cell proliferation and normal epithelial repair.

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