Fig. 3

Fig. 3 Control of LTCC current (ICa,L) and Cav?1c (L-type calcium channel alpha-1C subunit) protein levels by LITAF (lipopolysaccharide-induced tumor necrosis factor) in 3-wk-old cardiomyocytes. Cardiomyocytes were transduced with adenovirus encoding GFP (green fluorescence protein) or HA (hemagglutinin)-LITAF for 48 h. A, Left, voltage steps to measure I-V for ICa,L. Right, representative recordings of ICa,L in cardiomyocytes. B, Voltage dependence of ICa,L current density in cardiomyocytes transduced with GFP or LITAF (cells from 5 animals; mean±SEM; Student t test, P<0.05). C, Protein levels of Cav?1c, HA-LITAF, and tubulin ( left). Respective change in Cav?1c abundance, normalized to tubulin (n=5 animals, performed in triplicate; mean±SEM). Student t test, P<0.05 ( right). D, Current-voltage relationships of ICa,L peak currents for baseline conditions from cells expressing scrambled RNA or short hairpin RNA (shRNA) against endogenous LITAF (cells from 5 animals; mean±SEM; Student t test, P<0.05). E, Protein levels of Cav?1c, total LITAF, and tubulin ( left). Respective changes in Cav?1c and LITAF abundance, normalized to tubulin (n=5 animals, performed in triplicate; right).