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Fig. 2 Attenuation of Ca2+ transients and Cavα1c (L-type calcium channel alpha-1C subunit) abundance by LITAF (lipopolysaccharide-induced tumor necrosis factor) in adult rabbit cardiomyocytes. Cardiomyocytes were transduced with adenovirus expressing GFP (green fluorescence protein) or HA (hemagglutinin)-LITAF. A, Representative confocal line-scan images and corresponding Fluo-3 F/F0 time-dependent profiles at 1 Hz. B, Histograms depict mean data from Ca2+ transient amplitudes (GFP, 1.78±0.16 vs LITAF, 1.2±0.13 ΔF/F0), caffeine transient amplitudes (GFP, 2.8±0.15 vs LITAF, 2.1±0.19 ΔF/F0), fractional release and rates of Ca2+ removal by NCX (Na+/Ca2+ exchanger; kcaff), and SERCA2 (sarco/endoplasmic reticulum Ca2+-ATPase 2; kSR). Student t test, P<0.05 (2-3 heart preparations). C, Adult rabbit cardiomyocytes lysates were probed with anti-Cavα1c, anti-HA, and anti-GAPDH to indicate Cavα1c, exogenous LITAF and GAPDH (loading control) protein levels. D, Respective change in Cavα1c abundance, normalized to GAPDH (n=5 animals, performed in triplicate; mean±SEM). Student t test, P<0.05.