SLC7A11 Silencing Modulates Ferroptosis and Autophagy to Reduce Sodium Arsenite-Induced Activation of Hepatic Stellate Cells DOI Open Access

Wenmeng Ding,

Zhao Lijun,

Fei Huang

и другие.

Опубликована: Июнь 17, 2024

Arsenic is a prevalent environmental pollutant with recognized carcinogenic properties. Liver fibrosis frequent consequence of arsenic poisoning, the activation hepatic stellate cells (HSCs) being central event. Solute Carrier Family 7 Member 11 (SLC7A11), pivotal regulator ferroptosis, may be involved in process arsenic-induced liver fibrosis. This study utilized lentiviral vector-mediated SLC7A11 silencing LX-2 (a type human cells) to establish an knockout cell model, which was then exposed sodium arsenite (NaAsO2). Protein interactions were assessed through Immunoprecipitation (IP), and protein levels evaluated via Western blot analysis. It found that NaAsO2 decreased cellular Fe2+ nuclear receptor co-activator 4 (NCOA4) expression, reversing these effects. Additionally, IP analysis revealed interaction between Beclin1 proteins NaAsO2. Silencing attenuated reduction Tumor p53(P53), p-mammalian target rapamycin (p-mTOR) levels, along rise Beclin1, Phosphorylated adenosine monophosphate activated kinase (p-AMPK), α-smooth muscle actin (α-SMA) Fibroblast protein-α (FAP) induced by Consequently, promoted reduced autophagy P53/AMPK/mTOR pathway, inhibited HSC NaAsO2, potentially mitigating

Язык: Английский

SLC7A11 Silencing Modulates Ferroptosis and Autophagy to Reduce Sodium Arsenite-Induced Activation of Hepatic Stellate Cells DOI Open Access

Wenmeng Ding,

Zhao Lijun,

Fei Huang

и другие.

Опубликована: Июнь 17, 2024

Arsenic is a prevalent environmental pollutant with recognized carcinogenic properties. Liver fibrosis frequent consequence of arsenic poisoning, the activation hepatic stellate cells (HSCs) being central event. Solute Carrier Family 7 Member 11 (SLC7A11), pivotal regulator ferroptosis, may be involved in process arsenic-induced liver fibrosis. This study utilized lentiviral vector-mediated SLC7A11 silencing LX-2 (a type human cells) to establish an knockout cell model, which was then exposed sodium arsenite (NaAsO2). Protein interactions were assessed through Immunoprecipitation (IP), and protein levels evaluated via Western blot analysis. It found that NaAsO2 decreased cellular Fe2+ nuclear receptor co-activator 4 (NCOA4) expression, reversing these effects. Additionally, IP analysis revealed interaction between Beclin1 proteins NaAsO2. Silencing attenuated reduction Tumor p53(P53), p-mammalian target rapamycin (p-mTOR) levels, along rise Beclin1, Phosphorylated adenosine monophosphate activated kinase (p-AMPK), α-smooth muscle actin (α-SMA) Fibroblast protein-α (FAP) induced by Consequently, promoted reduced autophagy P53/AMPK/mTOR pathway, inhibited HSC NaAsO2, potentially mitigating

Язык: Английский

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