title: Loss of PPARγ expression by fibroblasts enhances dermal wound closure.
abstract: BACKGROUND
  Peroxisome proliferator-activated receptor (PPAR)γ may be a key regulator of connective tissue deposition and remodeling in vivo. PPARγ expression is reduced in dermal fibroblasts isolated from fibrotic areas of scleroderma patients; PPARγ agonists suppress the persistent fibrotic phenotype of this cell type. Previously, we showed that loss of PPARγ expression in fibroblasts resulted in enhanced bleomycin-induced skin fibrosis. However, whether loss of PPARγ expression in skin fibroblasts affects cutaneous tissue repair or homeostasis is unknown.
  
  
  RESULTS
  Mice deleted for PPARγ in skin fibroblasts show an enhanced rate of dermal wound closure, concomitant with elevated phosphorylation of Smad3, Akt and ERK, and increased expression of proliferating cell nuclear antigen (PCNA), collagen, α-smooth muscle actin (α-SMA) and CCN2. Conversely, dermal homeostasis was not appreciably affected by loss of PPARγ expression.
  
  
  CONCLUSIONS
  PPARγ expression by fibroblasts suppresses cutaneous tissue repair. In the future, direct PPARγ antagonists and agonists might be of clinical benefit in controlling chronic wounds or scarring, respectively.
authors.affiliation: Department of Dentistry, Schulich School of Medicine and Dentistry, Western University, Dental Sciences Bldg,, London, ON, N6A 5C1, Canada. Andrew.leask@schulich.uwo.ca.
authors.forename: Wei
authors.initials: W
authors.lastname: Sha
authors.forename: Katherine
authors.initials: K
authors.lastname: Thompson
authors.forename: Jennifer
authors.initials: J
authors.lastname: South
authors.forename: Murray
authors.initials: M
authors.lastname: Baron
authors.forename: Andrew
authors.initials: A
authors.lastname: Leask