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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Panax ginseng metabolite (GIM-1) modulates the effects of monobutyl phthalate (MBP) on the GPR30/GPER1 canonical pathway in human Sertoli cells

Texto completo
Autor(es):
de Freitas, Andre Teves A. G. [1] ; Pinho, Cristiane Figueiredo [1] ; Aquino, Ariana Musa [1] ; Domeniconi, Raquel Fantin [1] ; Justulin, Luis Antonio [1] ; Scarano, Wellerson Rodrigo [1]
Número total de Autores: 6
Afiliação do(s) autor(es):
[1] Sao Paulo State Univ UNESP, Inst Biosci, Dept Struct & Funct Biol, BR-18618970 Botucatu, SP - Brazil
Número total de Afiliações: 1
Tipo de documento: Artigo Científico
Fonte: REPRODUCTIVE TOXICOLOGY; v. 96, p. 209-215, SEP 2020.
Citações Web of Science: 1
Resumo

This study was performed to evaluate the effect of monobutyl phthalate (MBP) on GPR30-activated pathways in Sertoli cells. Additionally, we tested if GIM-1 (Panax ginseng metabolite) modulates MBP action. Human Sertoli cells (HSeC lineage) were exposed to MBP and/or GIM-1 for 30 min, 1, 12, and 48 h. Four experimental treatments were performed: control (DEMEM/F12 medium), MBP, GIM-1, and MBP + GIM-1. The results indicate that MBP activates GPR30, PKA, Src, EGFR, and the ERK1/2 proteins, while GIM-1 inhibits PKA, Src, ERK1/2, and the AKT pathway. MBP also enhances Cofilin expression, decreasing F-actin intensity on the cell surface in a short time. The combined exposure demonstrated a functional antagonism between compounds. Collectively, these data show that MBP activates GPR30 in Sertoli cells, and GIM-1 modulates this response, playing a protective role in Sertoli cells exposed to MBP. (AU)

Processo FAPESP: 12/00253-3 - Análise do padrão de metilação das regiões controladoras de imprinting dos genes H19 e IGF2 e da resposta androgênica em células de Sertoli humanas expostas ao TCDD (2,3,7,8-tetraclorodibenzeno-p-dioxina)
Beneficiário:Wellerson Rodrigo Scarano
Modalidade de apoio: Auxílio à Pesquisa - Regular