info:eu-repo/semantics/article
Estradiol stimulates cell proliferation via classic estrogen receptor-alpha and G protein-coupled estrogen receptor-1 in human renal tubular epithelial cell primary cultures
Fecha
2019-04Registro en:
Sanchez, Daiana Soledad; Fischer Sigel, Lilian Karina; Azurmendi, Pablo Javier; Vlachovsky, Sandra Gabriela; Oddo, Elisabet Mónica; et al.; Estradiol stimulates cell proliferation via classic estrogen receptor-alpha and G protein-coupled estrogen receptor-1 in human renal tubular epithelial cell primary cultures; Academic Press Inc Elsevier Science; Biochemical and Biophysical Research Communications; 512; 2; 4-2019; 170-175
0006-291X
CONICET Digital
CONICET
Autor
Sanchez, Daiana Soledad
Fischer Sigel, Lilian Karina
Azurmendi, Pablo Javier
Vlachovsky, Sandra Gabriela
Oddo, Elisabet Mónica
Armando, Inés
Ibarra, Fernando Raúl
Silberstein, Claudia Marcela
Resumen
This work was aimed to determine the effect of 17β-estradiol (17βE) on cell proliferation in human renal tubular epithelial cells (HRTEC) isolated from kidneys from pediatric subjects, as well as the role of estrogen receptors involved in the 17βE proliferative response. Treatment with 17βE (10 nmol/L, 24 h) significantly stimulated cell proliferation, measured by 5-bromo-2-deoxyuridine (BrdU) uptake, in HRTEC primary cultures and in tubular structures obtained by 3D cultured-HRTEC. Incubation of HRTEC with the G protein-coupled estrogen receptor 1 (GPER-1) agonist G-1 increased BrdU uptake. Incubation of HRTEC with 17βE activated the classic estrogen receptor alpha (ERα) but not ERβ. Treatment of HRTEC with the GPER-1 antagonist G-15, the ER inhibitor ICI182,780, or the β-catenin inhibitor iCRT14, completely abrogated the increase in BrdU uptake induced by 17βE. We also show that 17βE stimulated β-catenin protein expression and translocation to the nucleus of HRTEC, effects that were abrogated by G-15 and ICI 182,780. In conclusion, estradiol stimulates cell proliferation in HRTEC primary cultures through both ERα and GPER-1 estrogen receptors and involves β-catenin activation.