help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Published ahead of print on July 14, 2005, doi:10.1164/rccm.200410-1398OC
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Online Supplement
Right arrow All Versions of this Article:
200410-1398OCv1
172/8/1013    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Voynow, J. A.
Right arrow Articles by Proia, A. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Voynow, J. A.
Right arrow Articles by Proia, A. D.
American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 1013-1018, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200410-1398OC

Basal-like Cells Constitute the Proliferating Cell Population in Cystic Fibrosis Airways

Judith A. Voynow, Bernard M. Fischer, Bruce C. Roberts and Alan D. Proia

Departments of Pediatrics and Pathology, Duke University Medical Center, Durham, North Carolina

Correspondence and requests for reprints should be addressed to Judith A. Voynow, M.D., Pediatric Pulmonary Medicine, Box 2994, Duke University Medical Center, Durham, NC. E-mail: voyno001{at}mc.duke.edu

Rationale: Cystic fibrosis airways are recurrently exposed to noxious stimuli, leading to epithelial injury. Previous reports suggest that cystic fibrosis airway epithelia may respond to injury by increasing proliferation.

Objectives: We sought to determine the characteristics of the proliferating cell population in cystic fibrosis airways.

Methods: Six cystic fibrosis and six normal lung sections from lung transplant recipients or lung surgery were obtained from the Duke Hospital pathology archives. Sections containing bronchi were evaluated for epithelial cell proliferation using immunohistochemistry for a nuclear proliferation antigen, Ki-67, and image analysis; immunohistochemistry for basal cells using a cytokeratin 5/14 antibody; and immunohistochemistry for the epidermal growth factor receptor and ErbB2, two receptor tyrosine kinases implicated in epithelial proliferation and differentiation.

Results: Overall, cystic fibrosis sections had a greater proliferation index than control sections with 25.1 ± 2.1% positively staining nuclei/total nuclei compared with control sections, 4.6 ± 0.9% (p = 0.002). In cystic fibrosis sections only, there were areas of hyperplastic cuboidal cells adjacent to normal pseudostratified columnar epithelial sections; in these areas of epithelial hyperplasia, there was uniform Ki-67 staining, indicating a zone of proliferating cells. The proliferating cell population also expressed the basal cell cytokeratins 5/14 and epidermal growth factor receptor. Expression of ErbB2 was diminished in the proliferating cells.

Conclusions: Our results suggest that basal-like cells, expressing the epidermal growth factor receptor, constitute the proliferating cell population in cystic fibrosis airways.

Key Words: epidermal growth factor receptor • epithelial repair • ErbB2 • Ki-67




This article has been cited by other articles:


Home page
 Am. J. Respir. Cell Mol. Bio.Home page
T. N. Hilliard, J. Zhu, R. Farley, S. Escudero-Garcia, B. J. Wainwright, P. K. Jeffery, U. Griesenbach, A. Bush, J. C. Davies, and E. W. F. W. Alton
Nasal Abnormalities in Cystic Fibrosis Mice Independent of Infection and Inflammation
Am. J. Respir. Cell Mol. Biol., July 1, 2008; 39(1): 19 - 25.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
W. D. Hardie, C. Davidson, M. Ikegami, G. D. Leikauf, T. D. Le Cras, A. Prestridge, J. A. Whitsett, and T. R. Korfhagen
EGF receptor tyrosine kinase inhibitors diminish transforming growth factor-{alpha}-induced pulmonary fibrosis
Am J Physiol Lung Cell Mol Physiol, June 1, 2008; 294(6): L1217 - L1225.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
H. W. J. Young, O. W. Williams, D. Chandra, L. K. Bellinghausen, G. Perez, A. Suarez, M. J. Tuvim, M. G. Roy, S. N. Alexander, S. J. Moghaddam, et al.
Central Role of Muc5ac Expression in Mucous Metaplasia and Its Regulation by Conserved 5' Elements
Am. J. Respir. Cell Mol. Biol., September 1, 2007; 37(3): 273 - 290.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
A. Ibricevic, A. Pekosz, M. J. Walter, C. Newby, J. T. Battaile, E. G. Brown, M. J. Holtzman, and S. L. Brody
Influenza virus receptor specificity and cell tropism in mouse and human airway epithelial cells.
J. Virol., August 1, 2006; 80(15): 7469 - 7480.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
F. J. Accurso
Update in cystic fibrosis 2005.
Am. J. Respir. Crit. Care Med., May 1, 2006; 173(9): 944 - 947.
[Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
S. M. Casalino-Matsuda, M. E. Monzon, and R. M. Forteza
Epidermal Growth Factor Receptor Activation by Epidermal Growth Factor Mediates Oxidant-Induced Goblet Cell Metaplasia in Human Airway Epithelium
Am. J. Respir. Cell Mol. Biol., May 1, 2006; 34(5): 581 - 591.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2005 American Thoracic Society 		  Solid Organ Transplant for the Intensivist 2008