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ASBT inhibition alleviates cholangiopathy and hepatic fibrosis development in Cyp2c70-/- mice

ABSTRACT: ASBT inhibition alleviates cholangiopathy and hepatic fibrosis development in Cyp2c70-/- mice

PROVIDER: PRJNA759789 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15698631_1.fastq.gz	Fastqsanger.gz
	SRR15698631_2.fastq.gz	Fastqsanger.gz
	SRR15698632_1.fastq.gz	Fastqsanger.gz
	SRR15698632_2.fastq.gz	Fastqsanger.gz
	SRR15698633_1.fastq.gz	Fastqsanger.gz

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ASBT inhibition alleviates cholangiopathy and hepatic fibrosis development in Cyp2c70-/- mice

Project description:RNA-seq was used to compare the liver gene differentiation between WT and Cyp2c70-/- mice fed with chow and SC-435 containing diet. We aimed to characterize the cholestatic liver phenotype in the Cyp2c70 -/- mouse and test whether ASBT inhibition reduced injury.

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Effect of pharmacological inhibition of ASBT on bile composition and sclerosing cholangitis in mdr2 knockout mice

Project description:We report the effect of a potent pharmacological inhibition of ASBT in mdr2 -/- mice, compared to genetic and treatment controls using RNA-sequencing. Through quantification of mRNA in liver samples, we found significant upregulation of anti-inflammatory and anti-fibrotic gene signatures in mdr2-/- mice. Additionally, we report downregulation of pro-inflammatory genes invovled in leukocyte recruitment. Mdr2 knockout mice (female, 30 day old) were fed high fat-chow diet containing a potent inhibitor of ASBT for 14 days. Genotypic and dietary controls were included. RNA-sequencing was performed on liver samples taken from the caudate lobe.

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A natural small molecule alleviates liver fibrosis by targeting apolipoprotein L2

Project description:Liver fibrosis is an urgent clinical problem without effective treatment. Herein, we conduct a high-content screening on a natural “privileged” diterpenoid library to identify a potent anti-liver fibrosis lead DP. Leveraging photoaffinity labeling approach, apolipoprotein L2 (APOL2), an ER-rich protein, is identified as the direct target of DP. APOL2 is mainly expressed in activated hepatic stellate cells (HSCs) and could activate HSCs to synthesize ECM proteins. It can be induced by TGF-b1 and be antagonized by DP. Mechanistically, upon TGF-b1 stimulation, APOL2 binds ER Ca2+ pump SERCA2 to trigger ER stress, elevating its downstream PERK-HES1 axis to promote liver fibrosis, mildly dependent on the canonical TGF-b/Smad signaling. As a result, ablation of APOL2 significantly alleviates TGF-b1-stimulated HSCs activation, and abolishes anti-fibrosis effect of DP. Our findings not only define APOL2 as a novel therapeutic target for liver fibrosis, but also highlight DP as a promising lead for treatment of this symptom.

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Histone deacetylase inhibitor givinostat alleviates liver fibrosis by regulating hepatic stellate cell activation

Project description:Hepatic fibrosis, a common pathological manifestation of chronic liver injury, is generally considered to be the end result of an increase in extracellular matrix produced by activated hepatic stellate cells (HSCs). Targeting the mechanisms underlying HSC activation may provide a powerful therapeutic strategy for the prevention and treatment of liver fibrosis. A high-throughput screening assay was established, and the histone deacetylase inhibitor givinostat was identified as a potent inhibitor of HSC activation in vitro. Givinostat significantly inhibited HSC activation in vivo, ameliorated carbon tetrachloride-induced mouse liver fibrosis and lowered plasma aminotransferases. Transcriptomic analysis revealed the most significantly regulated genes in the givinostat treatment group in comparison with those in the solvent group, among which, Dmkn, Msln and Upk3b were identified as potential regulators of HSC activation. Givinostat significantly reduced the mRNA expression of Dmkn, Msln and Upk3b in both a mouse liver fibrosis model and in HSC-LX2 cells. Knocking down any of the aforementioned genes inhibited the TGF-β1-induced expression of α-smooth muscle actin and collagen type I, indicating that they are crucial for HSC activation. In summary, using a novel strategy targeting HSC activation, the present study identified a potential epigenetic drug for the treatment of hepatic fibrosis and revealed novel regulators of HSC activation.

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