Contractile Activity Regulates Inducible Nitric Oxide Synthase Expression and
NOi Production in Cardiomyocytes via a FAK-Dependent Signaling Pathway
Figure 5
Rescue of BDM inhibition of iNOS expression by CD2-FAK and Myr-AKT. (a) NRVMs were pretreated with BDM (7.5 mM) for 24 h. To “rescue” the BDM inhibition of iNOS expression, some cells were then infected (48 h, 10 moi) with Adv-expressing neβgal, WT-FAK, CD2-FAK, WT-AKT, or Myr-AKT with continued exposure to BDM. Cell extracts (50 μg total protein per lane) were then separated by SDS-PAGE and Western blotting with antibodies specific for FAK, AKT, iNOS, and GAPDH. ((a) and (c)) The quantitative results of 5 experiments are depicted. * versus WT-FAK or WT-AKT cells. (d) NRVMs were treated with 7.5 mM BDM for 24 h. To “rescue” the BDM inhibition of NOi production, some cells were then infected (10 moi) with WT-AKT or Myr-AKT for 48 h with continued exposure to BDM. NOi was then measured using DAF-2 DA. The quantitative results of 5 experiments are depicted. * versus BDM, # versus WT-AKT. (e) A multicomponent signaling pathway that links mechanical load to AKT activation and downstream signaling to iNOS is depicted.
