SMAD3 and inflammatory bowel disease: By using a specific antisense oligonucleotide that hybridizes to Smad7 mRNA in a sequence-specific manner, thereby triggering RNase H1 activity, mRNA degradation, and protein inhibition, we were able to show that Smad7 knockdown in ex vivo organ cultures of IBD mucosal explants and LPMCs restored the TGF-β1-associated Smad3 signaling and suppressed the production of inflammatory cytokines (Monteleone et al., 2001).