AJP - Lung Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol (September 15, 2006). doi:10.1152/ajplung.00049.2006
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
292/1/L232    most recent
00049.2006v1
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 Similar articles in PubMed
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 Samuelsen, J. T
Right arrow Articles by Becher, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Samuelsen, J. T
Right arrow Articles by Becher, R.
Submitted on February 10, 2006
Accepted on September 12, 2006

Regulation of rat alveolar type 2 cell proliferation in vitro involves type II cAMP-dependent protein kinase

Jan T Samuelsen1*, Per E Schwarze2, Henrik S Huitfeldt3, Vibeke Thrane4, Marit Lag2, Magne Refsnes2, Ellen Skarpen3, and Rune Becher2

1 Nordic Institute of Dental Materials, Haslum, Norway; Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway
2 Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway
3 Institute of Pathology, Rikshospitalet University Hospital, Oslo, Norway
4 Poison information centre, Oslo, Norway

* To whom correspondence should be addressed. E-mail: jts{at}niom.no.

To elucidate the role of cAMP and different cAMP-dependent protein kinases (PKA; A-kinase) in lung cell proliferation, we investigated rat alveolar type 2 cell proliferation in relation to activation or inhibition of PKA and PKA regulatory subunits (RII-alpha and RI-alpha). Both the number of proliferating type 2 cells and the level of different regulatory subunits varied during seven days of culture. The cells exhibited a distinct peak of proliferation after 5 days of culture. This proliferation peak was preceded by a rise in RII-alpha protein level. In contrast, an inverse relationship between RI-alpha and type 2 cell proliferation was noted. Activation of PKA increased type 2 cell proliferation if given at peak RII-alpha expression. Furthermore, PKA inhibitors lowered the rate of proliferation only when a high RII level was observed. An antibody against the anchoring region of RII-alpha showed cell cycle dependent binding in contrast to antibodies against other regions, possibly related to altered binding to A-kinase anchoring protein (AKAP). Following activation of PKA, relocalisation of RII-alpha was confirmed by immunocytochemistry. In conclusion, it appears that activation of PKA II is important in regulation of alveolar type 2 cell proliferation.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
L. M. Marsh, L. Cakarova, G. Kwapiszewska, W. von Wulffen, S. Herold, W. Seeger, and J. Lohmeyer
Surface expression of CD74 by type II alveolar epithelial cells: a potential mechanism for macrophage migration inhibitory factor-induced epithelial repair
Am J Physiol Lung Cell Mol Physiol, March 1, 2009; 296(3): L442 - L452.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
L. P. Desai, K. E. Chapman, and C. M. Waters
Mechanical stretch decreases migration of alveolar epithelial cells through mechanisms involving Rac1 and Tiam1
Am J Physiol Lung Cell Mol Physiol, November 1, 2008; 295(5): L958 - L965.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.