AJP - Lung AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol (January 4, 2002). doi:10.1152/ajplung.00308.2001
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/1/L12    most recent
00308.2001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hastings, R. H
Right arrow Articles by Deftos, L. J
Right arrow Search for Related Content
PubMed
Right arrow Articles by Hastings, R. H
Right arrow Articles by Deftos, L. J

Articles in PresS, published online ahead of print January 4, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00308.2001
Submitted on August 7, 2001
Accepted on December 21, 2001

Parathyroid hormone-related protein 38-64 regulates lung cell proliferation after silica injury

Randolph H Hastings1*, Angela Asirvatham2, Rick Quintana3, Rebeca Sandoval3, Ruchika Dutta3, Douglas W Burton4, and Leonard J Deftos5

1 Anesthesiology, VA San Diego Healthcare System, San Diego, CA, USA; Anesthesiology, University of California, San Diego, San Diego, CA, USA
2 Anesthesiology, University of California, San Diego, San Diego, CA, USA
3 Research, VA San Diego Healthcare System, San Diego, CA, USA
4 Medicine, University of California, San Diego, San Diego, CA, USA; Research, VA San Diego Healthcare System, San Diego, CA, USA
5 Medicine, VA San Diego Healthcare System, San Diego, CA, USA; Medicine, University of California, San Diego, San Diego, CA, USA

* To whom correspondence should be addressed. E-mail: rhhastings{at}ucsd.edu.

Inhalation of silica leads to acute lung injury and alveolar type II cell proliferation. Type II cell proliferation after hyperoxic lung injury is regulated, in part, by parathyroid hormone-related protein (PTHrP). In this study, we investigated lung PTHrP and its effects on epithelial proliferation after injury induced by silica. Lung PTHrP decreased modestly four days after instilling 10 mg silica into rat lungs and then recovered from four to 28 days. The number of proliferating cell nuclear antigen (PCNA)-positive type II cells was increased three-fold in silica-injured lungs compared to controls. Subsequently, rats were treated with four exogenous PTHrP peptides in the silica instillate and administered sc daily. One peptide, PTHrP 38-64, had consistent and significant effects on cell proliferation. PTHrP 38-64 increased the median number of PCNA-positive cells/field nearly four-fold above controls, 380 vs. 109 (P < 0.05). Thymidine incorporation was 2.5 times higher in type II cells isolated from rats treated with PTHrP 38-64 compared to PBS. PTHrP 38-64 significantly increased the number of cells expressing alkaline phosphatase, a type II cell marker. This study indicates that PTHrP 38-64 stimulates type II cell growth and may have a role in lung repair in silica-injured rats.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
R. H. Hastings, R. A. Quintana, R. Sandoval, D. W. Burton, and L. J. Deftos
Amino-terminal and midmolecule parathyroid hormone-related protein, phosphatidylcholine, and type II cell proliferation in silica-injured lung
Am J Physiol Lung Cell Mol Physiol, December 1, 2003; 285(6): L1312 - L1322.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2002 by the American Physiological Society.