MedElevator
Войти в исследования Life sciences · 2026
Nuclear translocation of GPS2 promotes activation of hepatic stellate cells by fatty acid oxidation pathway.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hong Haiqin, Wang Li, Lu Muran, An Ziyi, Shi Yanxia, Deng Qi, Wu Jingjing, Wang Benwei, Lu Jialu, Li Mengjun, Huang Yan, Lu Weili, Wu Fanrong
Аннотация
AIMS: To investigate the role of G protein pathway suppressor 2 (GPS2) nuclear translocation in hepatic stellate cell (HSC) activation and its underlying mechanisms in liver fibrosis.
MATERIALS AND METHODS: RNA sequencing (RNA-seq) was performed to analyze differential gene expression among experimental groups. Fatty acid oxidation (FAO) was evaluated using FAO Blue staining. Co-immunoprecipitation (Co-IP) assays were conducted to investigate the interaction between GPS2 and its potential binding partners. In addition, HSC activation was induced by PDGF-BB, and cell proliferation, activation markers, and mitochondrial FAO levels were systematically assessed.
KEY FINDINGS: GPS2 nuclear translocation was significantly increased during HSC activation. Inhibition of GPS2 nuclear translocation attenuated liver fibrosis and reduced HSC activation. Mechanistically, blocking GPS2 nuclear translocation weakened its interaction with PPARα. PPARα was found to regulate mitochondrial FAO, which in turn promoted HSC proliferation and activation. Suppression of PPARα reduced FAO and alleviated HSC activation.
SIGNIFICANCE: This study identifies a novel mechanism whereby GPS2 nuclear translocation promotes HSC activation through interaction with PPARα and regulation of mitochondrial FAO. Targeting GPS2 nuclear translocation may represent a potential therapeutic strategy for liver fibrosis.
MATERIALS AND METHODS: RNA sequencing (RNA-seq) was performed to analyze differential gene expression among experimental groups. Fatty acid oxidation (FAO) was evaluated using FAO Blue staining. Co-immunoprecipitation (Co-IP) assays were conducted to investigate the interaction between GPS2 and its potential binding partners. In addition, HSC activation was induced by PDGF-BB, and cell proliferation, activation markers, and mitochondrial FAO levels were systematically assessed.
KEY FINDINGS: GPS2 nuclear translocation was significantly increased during HSC activation. Inhibition of GPS2 nuclear translocation attenuated liver fibrosis and reduced HSC activation. Mechanistically, blocking GPS2 nuclear translocation weakened its interaction with PPARα. PPARα was found to regulate mitochondrial FAO, which in turn promoted HSC proliferation and activation. Suppression of PPARα reduced FAO and alleviated HSC activation.
SIGNIFICANCE: This study identifies a novel mechanism whereby GPS2 nuclear translocation promotes HSC activation through interaction with PPARα and regulation of mitochondrial FAO. Targeting GPS2 nuclear translocation may represent a potential therapeutic strategy for liver fibrosis.