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RNA Sequencing Analysis of Control and Blnc1 liver specific knockout mice (LKO) Liver Transcriptomes after 24 weeks NASH diet feeding

ABSTRACT: RNA Sequencing Analysis of Control and Blnc1 liver specific knockout mice (LKO) Liver Transcriptomes after 24 weeks NASH diet feeding

PROVIDER: PRJNA427816 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6427382.fastq.gz	Fastqsanger.gz
	SRR6427383.fastq.gz	Fastqsanger.gz
	SRR6427384.fastq.gz	Fastqsanger.gz
	SRR6427385.fastq.gz	Fastqsanger.gz
	SRR6427386.fastq.gz	Fastqsanger.gz

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RNA Sequencing Analysis of Control and Blnc1 liver specific knockout mice (LKO) Liver Transcriptomes after 24 weeks NASH diet feeding

Project description:Hepatic lipogenesis is a central aspect of the feeding response and is aberrantly induced in the progression of fatty liver disease. Liver X receptors (LXRs) and sterol regulatory element-binding protein 1c (SREBP1c) are potent activators of the lipogenic gene program that promote triglyceride synthesis and hepatic steatosis in the insulin-resistant state. To date, key protein components of the LXR-SREBP1c axis have been uncovered that mediate transcriptional activation of SREBP1c by LXRs and nutrient and hormonal regulation. However, whether this regulatory pathway interfaces with long noncoding RNAs (lncRNAs) remains largely unexplored. Here we show that hepatic expression of Blnc1, a regulator of brown adipocyte development, is strongly associated with adiposity and liver fat content in mice. Blnc1 is required for the induction of SREBP1c and hepatic lipogenic genes in response to LXR activation. CRISPR/Cas9-mediated liver-specific inactivation of Blnc1 abrogates high fat diet-induced hepatic steatosis and insulin resistance. We further observed that liver Blnc1 expression is elevated in a mouse model of nonalcoholic steatohepatitis (NASH). Mice lacking Blnc1 in the liver are protected from diet-induced NASH and exhibit attenuated liver injury, inflammation and liver fibrosis. At the molecular level, proteomic analysis of the Blnc1 ribonucleoprotein complex in the liver identified endothelial differentiation related factor 1 (EDF1) as a component of the LXR transcriptional complex that acts in concert with Blnc1 to stimulate SREBP1c expression. These findings uncover a lncRNA ribonucleoprotein complex that licenses obesity-linked activation of hepatic lipogenesis and NAFLD pathogenesis.

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Hepatic transcriptomic changes during non-alcoholic steatohepatitis (NASH)-associated liver carcinogenesis in mice

Project description:Hepatocellular carcinoma (HCC), which accounts for 90% of all primary livers tumors, is the fourth most common cancer in the world. The development of HCC is a long-term and complex process, and uncovering the molecular mechanisms associated with HCC development is critical for the disease diagnosis, prevention, and treatment. Exploring these mechanisms using human HCC samples is desirable, but frequently impractical, with a number of limitations and shortcomings. The STAMTM (Stelic Institute & Co, Tokyo, Japan) mouse model of NASH-associated liver carcinogenesis is considered a useful and relevant model for investigating the molecular pathogenesis of NASH-derived HCC. This model resembles the human HCC development associated with progression from simple steatosis to NASH, fibrosis, and HCC. In the present study, by using high-throughput whole genome microarrays (SurePrint G3 Mouse Gene Expression v2, 8x60K; Agilent Technologies, Santa Clara, CA), we examined the transcriptomic profiles in the livers of STAMTM mice at different stages of liver carcinogenesis, including steatosis (6 week time interval), NASH (8 weeks), fibrotic stage (12 weeks), and in full-fledged HCC (20 weeks). The results of microarray analyses showed significant progressive changes in hepatic gene expression during the development of HCC. A total of 970, 1462, 2742, and 2857 of differentially expressed genes were identified in the livers at 6, 8, 12, and 20 weeks, respectively. Detailed analysis of these differentially expressed genes will benefit the understanding of the underlying mechanisms of non-alcoholic fatty liver disease-derived HCC. Transcriptomic profile in the liver of STAM mice at 6 weeks (steatosis; n=3), 8 weeks (steatohepatitis; n=3) 12 weeks (fibrosis; n=4) and 20 weeks (HCC-stage tumor tissue, n=4) weeks. Age-matched control samples were also analyzed.

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Gene expression profile of liver obtained from liver-specific LPIAT1 KO (LKO) mice on chow or high fat diet (HFD).

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