Figure 2From: Estradiol promotes the development of a fibrotic phenotype and is increased in the serum of patients with systemic sclerosisEstradiol promotes fibronectin production via specific signaling cascades. (A) Fibronectin (FN) protein levels in the cellular lysates of normal skin fibroblasts. Normal skin fibroblasts were stimulated with 17β-estradiol (E2) for 48 hours in the presence or absence of the following chemical inhibitors: MEK inhibitor (MEKi), phosphoinositol 3-kinase inhibitor (PI3Ki), and p38 kinase inhibitor (p38Ki). Cellular lysates were analyzed by western blot using anti-EDA-FN, estrogen receptor (ER)α, ERβ, and GAPDH antibodies. (B) Effect of E2 ligands on the expression and deposition of FN in the extracellular matrix (ECM) of normal skin fibroblasts. PPT, propyl-pyrazole-triol. Primary fibroblasts were cultured with vehicle (dimethylsulfoxide (DMSO), ethanol (EtOH)), E2, PPT, or genistein for 48 hours. ECM was analyzed by western blot using anti-EDA-FN and anti-vitronectin antibodies. Ethanol was used as vehicle for E2 and PPT. DMSO was used as a vehicle for genistein.Back to article page