Abstract
Purpose: :
To determine whether or not troglitazone suppresses wound healing model in monolayer culture of the SV40- immortalized human corneal epithelial cell (HCEC) line. The perpxisome proliferation-activated receptor (PPAR) family consists of three members; PPAR-beta, -delta or -gamma which are involved in modulation of inflammatory cell function or cell proliferation during wound healing. Troglitazone is a ligand of PPAR-gamma.
Methods: :
Efects of Troglitazon on HCEC migration were examined subsequent to wounding confluent monolayer cultures. Alamar blue staining evaluated the effects of Troglitazone (0-10 microM) on HCEC proliferation. Immunostaining determined Smad3. One to 3 hours after wounding, Troglitazone inhibits nuclear translocation of Smad3 near the wound.
Results: :
Troglitazon suppressed wound-induced cell migration and proliferation. Injury-induced Smad nuclear translocalization was also suppressed by the compound in HCEC monolayer culture.
Conclusions: :
Troglitazone suppresses wound healing in cultured HCEC sheet. These findings suggest that PPAR-gamma play a role in TGFb-driven corneal epithelial cell migration.
Keywords: wound healing • signal transduction • proliferation