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. 2014 Jul 31;9(7):e103433. doi: 10.1371/journal.pone.0103433

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© 2014 You et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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A. Cells were transiently transfected with a dominant negative plasmid encoding Mal (DN-Mal) or empty vector (pDeNy, lane 2). Cell lysates were prepared, and samples were immunoblotted with an anti-HO-1 antibody. B. Cells were transfected with Mal siNRA or control siRNA, and then treated with MALP-2 (5 ng/ml) for 16 h. Expression of Mal and HO-1 were analyzed by Western blot. C. Cells were cotransfected with a DN-MyD88 or DN-Mal and HO-1-luc reporter gene, and then treated with MALP-2 for 8 h. The luciferase activity derived from HO-1 activation was normalized to the transfection efficiency with β-gal, and pDeNy was used as a control vector. All values are expressed as means ± SEM obtained from three independent experiments. *, P<0.05 and **, P<0.01 for significant difference between compared groups.