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Am J Physiol Lung Cell Mol Physiol 292: L232-L239, 2007. First published September 15, 2006; doi:10.1152/ajplung.00049.2006 Free Article
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Regulation of rat alveolar type 2 cell proliferation in vitro involves type II cAMP-dependent protein kinase

Jan T. Samuelsen,1,2 Per E. Schwarze,1 Henrik S. Huitfeldt,3 E. Vibeke Thrane,4 Marit Låg,1 Magne Refsnes,1 Ellen Skarpen,3 and Rune Becher1

1Norwegian Institute of Public Health, Division of Environmental Medicine, Oslo; 2Nordic Institute of Dental Materials, Haslum; 3Laboratory for Toxicopathology, Institute of Pathology, University of Oslo, Rikshospitalet University Hospital, Oslo; and 4Poison Information Centre, Oslo, Norway

Submitted 10 February 2006 ; accepted in final form 12 September 2006

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 7 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. Following activation of PKA, relocalization 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.

protein kinase A; A-kinase anchoring protein; lung


Address for reprint requests and other correspondence: J. T. Samuelsen, Nordic Institute of Dental Materials, PO Box 70, N-1305 Haslum, Norway (e-mail: jts{at}niom.no)






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