Smad7 deficiency enhances Ang II-induced NF-κB signaling activation, upregulation of Sp1, but loss of miR-29b.

<p>(A) Western blot analysis of phosphorylated IκBα. (B) Western blot analysis of phosphorylated NF-κB/p65. (C) Western blot analysis of Sp1. (D) Real-time PCR analysis of miR-29b expression. Results show that deletion of Smad7 enhances activation of NF-κB signaling by promoting phosphorylation of IκBα and p65, promotes Sp1 expression, but induces loss of cardiac miR-29b. Data represent the mean±SE for a group of 6 mice. *P<0.05, **P<0.01, ***P<0.001vs saline control; ^#P<0.05,^###P<0.001 vs Smad7 WT mice.