When regenerative processes cannot keep pace with cell death, functional epithelia are replaced by scar. Scarring is characterized by both excessive accumulation of fibrous matrix and persistent outgrowth of cell types that accumulate transiently during successful wound healing, including myofibroblasts (MFs) and progenitors. This suggests that signaling that normally directs these cells to repair injured epithelia is deregulated. To evaluate this possibility, we examined liver repair during different types of liver injury after Smoothened (SMO), an obligate intermediate in the Hedgehog (Hh) signaling pathway, was conditionally deleted in cells expressing the MF-associated gene, α
Gregory A. Michelotti, Guanhua Xie, Marzena Swiderska, Steve S. Choi, Gamze Karaca, Leandi Krüger, Richard Premont, Liu Yang, Wing-Kin Syn, Daniel Metzger, Anna Mae Diehl
Conditional disruption of SMO in αSMA+ cells inhibits Hh signaling in MFs.