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- W2967546593 endingPage "101302" @default.
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- W2967546593 abstract "Activation of hepatic stellate cells (HSC) is a hallmark event in liver fibrosis. Accumulation of reactive oxygen species (ROS) serves as a driving force for HSC activation. The regulatory subunits of the NOX complex, NCF1 (p47phox) and NCF2 (p67phox), are up-regulated during HSC activation contributing to ROS production and liver fibrosis. The transcriptional mechanism underlying NCF1/2 up-regulation is not clear. In the present study we investigated the role of serum response factor (SRF) in HSC activation focusing on the transcriptional regulation of NCF1/2. We report that compared to wild type littermates HSC-conditional SRF knockout (CKO) mice exhibited a mortified phenotype of liver fibrosis induced by thioacetamide (TAA) injection or feeding with a methionine-and-choline deficient diet (MCD). More importantly, SRF deletion attenuated ROS levels in HSCs in vivo. Similarly, SRF knockdown in cultured HSCs suppressed ROS production in vitro. Further analysis revealed that SRF deficiency resulted in repression of NCF1/NCF2 expression. Mechanistically, SRF regulated epigenetic transcriptional activation of NCF1/NCF2 by interacting with and recruiting the histone acetyltransferase KAT8 during HSC activation. In conclusion, we propose that SRF integrates transcriptional activation of NCF1/NCF2 and ROS production to promote liver fibrosis." @default.
- W2967546593 created "2019-08-22" @default.
- W2967546593 creator A5003872416 @default.
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- W2967546593 date "2019-09-01" @default.
- W2967546593 modified "2023-10-16" @default.
- W2967546593 title "Serum response factor (SRF) promotes ROS generation and hepatic stellate cell activation by epigenetically stimulating NCF1/2 transcription" @default.
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- W2967546593 doi "https://doi.org/10.1016/j.redox.2019.101302" @default.
- W2967546593 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6831835" @default.
- W2967546593 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31442911" @default.
- W2967546593 hasPublicationYear "2019" @default.
- W2967546593 type Work @default.