CLDN7 and colitis: Claudin-7 was identified as a novel substrate of MMP-7, and either active MMP-7 or Claudin-7 knockdown by siRNA increased Caco-2 monolayer permeability, which was further supported by studies with WT and Mmp7-/- mice showing that MMP-7 deficiency resulted in augmented intestinal barrier function and less severe colitis upon DSS insult.