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Effects of lutein on transforming growth factor-β2 induced epithelial-mesenchymal transition in ARPE-19 cells / 上海交通大学学报(医学版)
Journal of Shanghai Jiaotong University(Medical Science) ; (12): 571-577, 2019.
Artigo em Chinês | WPRIM | ID: wpr-843413
ABSTRACT
Objective • To establish the transforming growth factor-β2 (TGF-β2) induced epithelial-mesenchymal transition (EMT) model of retinal pigment epithelium cells, and investigate the effect and mechanism of lutein on EMT. Methods • ARPE-19 cells were cultured and divided into 4 groups including control group, TGF-β2 group, TGF-β2+lutein group and lutein group. The mRNA levels of α-smooth muscle actin (α-SMA), fibronectin (FN) and E-cadherin were analyzed by real-time PCR. The protein expression of α-SMA, FN and occludin were assayed by Western blotting. Immunofluorescence was used to detect the change of α-SMA. Meanwhile, Western blotting was performed to detect the expression levels of pSmad3 in the TGF/Smad signaling pathway. Results • TGF-β2 induced EMT was inhibited by lutein. Lutein decreased the mRNA and protein levels of the mesenchymal markers α-SMA and FN, and increased the expression of the epithelial markers E-cadherin and occludin (all P<0.05). Immunofluorescence showed that lutein can inhibit the conversion of epithelial cells into myofibroblasts. Lutein significantly downregulated the high expression of pSmad3 in TGF-β2 treated ARPE-19 cells (P=0.001). Conclusion • Lutein inhibits TGF-β2 induced EMT by downregulating the expression of pSmad3 in TGF-β/Smad signaling pathway, indicating it may attenuate subretinal fibrosis.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Journal of Shanghai Jiaotong University(Medical Science) Ano de publicação: 2019 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Journal of Shanghai Jiaotong University(Medical Science) Ano de publicação: 2019 Tipo de documento: Artigo