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  • Title: Regulation of rat alveolar type 2 cell proliferation in vitro involves type II cAMP-dependent protein kinase.
    Author: Samuelsen JT, Schwarze PE, Huitfeldt HS, Thrane EV, Låg M, Refsnes M, Skarpen E, Becher R.
    Journal: Am J Physiol Lung Cell Mol Physiol; 2007 Jan; 292(1):L232-9. PubMed ID: 16980378.
    Abstract:
    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 (RIIalpha and RIalpha). 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 RIIalpha protein level. In contrast, an inverse relationship between RIalpha and type 2 cell proliferation was noted. Activation of PKA increased type 2 cell proliferation if given at peak RIIalpha expression. Furthermore, PKA inhibitors lowered the rate of proliferation only when a high RII level was observed. An antibody against the anchoring region of RIIalpha 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 RIIalpha was confirmed by immunocytochemistry. In conclusion, it appears that activation of PKA II is important in regulation of alveolar type 2 cell proliferation.
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