Mauro B Ruffy1, Shaun S Kunnavatana, R James Koch. 1. Wound Healing and Tissue Engineering Laboratory, Department of Otolaryngology-Head and Neck Surgery, Stanford University Medical Center, Stanford, CA, USA.
Abstract
OBJECTIVE: To evaluate the effects of tamoxifen on the growth and autocrine growth factor production of human dermal fibroblasts from the face. METHODS: In vitro study of normal adult dermal fibroblast cells developed from surgical specimens in a serum-free model. Cell cultures were exposed to 5-, 8-, 12-, 16-, and 50-microg/mL concentrations of tamoxifen solution. Cell counts were performed, and the cell-free supernatants were collected at 0, 1, 3, 5, and 7 days after the initial exposure. Population doubling times were calculated, and supernatants were quantitatively assayed for basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), and transforming growth factor (TGF) beta1. RESULTS: Tamoxifen appears to delay cellular proliferation rates in a dose-dependent manner up to a concentration of 12 microg/mL. Higher concentrations, approaching 50 microg/mL, appear to have a toxic effect on cell growth. The analysis of growth factor production revealed decreased levels of bFGF and VEGF but no change in the levels of TGF-beta1. CONCLUSIONS: The in vitro findings of delayed cell proliferation and decreased production of VEGF and bFGF in cells exposed to tamoxifen are consistent with previous in vivo reports of delayed wound healing but improved scar formation. The in vitro findings of growth factor modulation by tamoxifen provide cellular and molecular evidence supporting the clinical use of tamoxifen to ultimately improve scar formation.
OBJECTIVE: To evaluate the effects of tamoxifen on the growth and autocrine growth factor production of human dermal fibroblasts from the face. METHODS: In vitro study of normal adult dermal fibroblast cells developed from surgical specimens in a serum-free model. Cell cultures were exposed to 5-, 8-, 12-, 16-, and 50-microg/mL concentrations of tamoxifen solution. Cell counts were performed, and the cell-free supernatants were collected at 0, 1, 3, 5, and 7 days after the initial exposure. Population doubling times were calculated, and supernatants were quantitatively assayed for basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), and transforming growth factor (TGF) beta1. RESULTS:Tamoxifen appears to delay cellular proliferation rates in a dose-dependent manner up to a concentration of 12 microg/mL. Higher concentrations, approaching 50 microg/mL, appear to have a toxic effect on cell growth. The analysis of growth factor production revealed decreased levels of bFGF and VEGF but no change in the levels of TGF-beta1. CONCLUSIONS: The in vitro findings of delayed cell proliferation and decreased production of VEGF and bFGF in cells exposed to tamoxifen are consistent with previous in vivo reports of delayed wound healing but improved scar formation. The in vitro findings of growth factor modulation by tamoxifen provide cellular and molecular evidence supporting the clinical use of tamoxifen to ultimately improve scar formation.
Authors: Lauro R Soares-Lopes; Ione M Soares-Lopes; Lauro Ll Filho; Airlane P Alencar; Benedito B da Silva Journal: Exp Biol Med (Maywood) Date: 2017-03-17
Authors: Humberto Dellê; José Roberto C Rocha; Rita C Cavaglieri; José Mauro Vieira; Denise M A C Malheiros; Irene L Noronha Journal: J Am Soc Nephrol Date: 2011-11-03 Impact factor: 10.121