Data associated with the publication: Localized knockout of E-cadherin in subglottic mucosa increases fibrosis

We previously reported that iSGS patients have decreased expression of the tight junction protein E-cadherin in the fibrotic region of their tracheas. We demonstrated that epithelial cells from iSGS patients had increased permeability in vitro which we believe contributes to this fibrotic disease. In order to futher confirm the E-cadherin in the development of tracheal stenosis we utilized an E-cadherin flox mouse and exposed the tracheas to Adenovirus expressing CRE using a hydrogel delivery system. Loss of E-cadherin lead to increased fibrotic development in a mouse model of tracheal stenosis with significantly increased lamina propria thickness, increased mortality, and increased expression of pro-fibrotic genes.