Expression data from 7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKβ

We found genetic deletion of IKKβ in mdx cardiomyocytes improved cardiac function and normalized calcium transients. We used microarrays to profile gene expression in hearts of mdx mice with intact IKKβ signaling and hearts of mdx mice with IKKβ-deficient cardiomyocytes to identify genes differentially regulated by NF-[kappa]B. signaling in dystrophic hearts. mdx mice conditionally deleted for IKKβ specifically in cardiomyocytes were created crossing IKKβ floxed mdx mice with mdx mice positive for the alpha myosin heavy chain (Myh6) promoter driving cre recombinase. Myh6 cre positive mice were our experimental mice and denoted “mdx heart Myh6-cre;IKKβ[delta]. Age matched littermates without the cardiac-specific Myh6 cre were our controls and denoted “mdx heart IKKβf/f”. RNA was prepared from 7-month-old whole hearts. 7 total samples were analyzed, 4 experimental and 3 control.