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. 2010 May 26;15(5):1109–1121. doi: 10.1111/j.1582-4934.2010.01095.x

fig 2.

fig 2

Rac1 enhances LPS-induced TNF-α expression in neonatal cardiomyocytes. WT cardiomyocytes were infected with Ad-GFP or Ad-Rac1N17 for 24 hrs. Cardiomyocytes were treated with LPS (1 μg/ml) for 3 or 5 hrs. TNF-α mRNA (A) and TNF-α protein in culture medium (B) were measured by real-time RT-PCR and ELISA, respectively. Neonatal cardiomyocytes from Rac1f/f mice were infected with Ad-GFP and Ad-Cre for 24 hrs. Rac1 protein was measured by Western blot analysis (C). Rac1f/f cells, infected with Ad-GFP or Ad-Cre, were treated with LPS for 3 or 5 hrs. TNF-α mRNA (D) and TNF-α protein in culture medium (E) were measured as described above. Data are means ± S.E.M. from three to seven independent experiments. **P < 0.01 versus Ad-GFP; †P < 0.05, ††P < 0.01 versus Ad-GFP+LPS.