help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH

Published ahead of print on July 21, 2005, doi:10.1165/rcmb.2004-0319OC

Am. J. Respir. Cell Mol. Biol., Volume 33, Number 4, October 2005, 371-377

A more recent version of this article appeared on October 1, 2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2004-0319OCv1
33/4/371    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 Kuang, P.-P.
Right arrow Articles by Goldstein, R. H
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kuang, P.-P.
Right arrow Articles by Goldstein, R. H

Submitted on October 8, 2004
Revised on July 15, 2005

Engraftment of Neonatal Lung Fibroblasts into the Normal and Elastase-injured Lung

Ping-Ping Kuang1, Edgar Lucey1, David C Rishikof1, Donald E Humphries2, Daniel Bronsnick1, and Ronald H Goldstein1*

1 Pulmonary Center, Boston University School Of Medicine, Boston, MA, USA, 2 Department of Research, Boston University School Of Medicine and the Boston VA Healthcare System, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: rgoldstein{at}lung.bumc.bu.edu.

Interstitial fibroblasts are an integral component of the alveolar wall. These cells produce matrix proteins that maintain the extracellular scaffold of alveolar structures. Emphysema is characterized by airspace enlargement resulting from the loss of alveolar cellularity and matrix. In this study, we explored the endotracheal delivery of fibroblasts to the lung parenchyma as a means of repairing damaged alveolar structures directly or indirectly for the delivery of transgenes. Fibroblasts were isolated from the lungs of neonatal transgenic mice expressing GFP during the period of rapid alveolarization. These GFP+ cells maintained their myofibroblast phenotype in culture and expressed elastin and {alpha}-smooth muscle actin mRNA. We administered GFP+ fibroblasts to saline- and elastase-treated mice by endotracheal instillation. We detected more GFP+ fibroblasts in the alveolar walls and in the interstitial areas of elastase- injured lungs than in normal lungs as assessed by immunohistochemistry and fluorescent imaging. The presence of GFP+ fibroblasts in the interstitium demonstrated transepithelial migration of these cells. Expression of GFP+ fibroblasts in recipient lungs was maintained for at least 20 days following endotracheal administration. These cells synthesize matrix components including elastin in vitro and could contribute to restoring the structural integrity of the alveolar wall.




This article has been cited by other articles:


Home page
Proc Am Thorac SocHome page
D. J. Weiss, J. K. Kolls, L. A. Ortiz, A. Panoskaltsis-Mortari, and D. J. Prockop
Stem Cells and Cell Therapies in Lung Biology and Lung Diseases
Proceedings of the ATS, July 15, 2008; 5(5): 637 - 667.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2005 American Thoracic Society.