PT  - JOURNAL ARTICLE
AU  - Hartmut Kuhn
AU  - Claudia Hänel
AU  - Stephan Hammerschmidt
AU  - Hubert Wirtz
TI  - Influence of protein kinase C on stretch-induced apoptosis in rat alveolar type II cells
DP  - 2012 Sep 01
TA  - European Respiratory Journal
PG  - P824
VI  - 40
IP  - Suppl 56
4099  - http://erj.ersjournals.com/content/40/Suppl_56/P824.short
4100  - http://erj.ersjournals.com/content/40/Suppl_56/P824.full
SO  - Eur Respir J2012 Sep 01; 40
AB  - Background: Cyclic stretching of alveolar type II (ATII) cells has been shown to induce apoptosis and is associated with alterations of F-actin cytoskeleton. Protein kinase C is able to promote alterations in the actin cytoskeleton.Objektives: We hypothesize that PKC is involved in the regulation of apoptosis in stretched cells. Therefore we investigated the PKC expression in stretched cells and their influence on actin cytoskeleton and stretch-induced apoptosis.Methods: Alveolar type II (ATII) cells were exposed to cyclic stretch using a stretching pattern characterized by frequency of 40 [min_1] and an amplitude of 30 [%]. After stretching we determined PKC-expression by Western blot. Next, we treated ATII cells with phorbol ester (PMA, a PKC stimulator), measured (a) F-actin by phalloidin staining, (b) elasticity with atomic force microscope (AFM), and (c) determined the effect of PMA on stretch-induced apoptosis using an Annexin V-FITC Apoptosis Detection Kit. Further, we tested the effect of the PKC inhibitor Staurosporin on stretch-induced apoptosis.Results: Our results showed an increase of PKC in stretched ATII cells after 1h. The stimulation of PKC with phorbol ester (PMA) induced a decrease of F-actin (21,5%) and elastic modulus (24,9%). We observed that treatment of ATII cells with PMA during stretching reduced the number of apoptotic cells (control 32,8%; PMA 16,1%). Inhibition of PKC using staurosporin increased the number of apoptotic cells (control 27,7%; Staurosporin 36,1%).Conclusions: We conclude that activation of PKC is able to prevent apoptosis in stretched cells. Remodelling of cytoskeleton to a softer cell by PKC seems to be a possible mechanism for it.