Sauchinone controls hepatic cholesterol homeostasis by the negative regulation of PCSK9 transcriptional network
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ABSTRACT:
PROVIDER: PRJNA450545 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7013800_1.fastq.gz | Fastqsanger.gz | |||
| SRR7013800_2.fastq.gz | Fastqsanger.gz | |||
| SRR7013801_1.fastq.gz | Fastqsanger.gz | |||
| SRR7013801_2.fastq.gz | Fastqsanger.gz | |||
| SRR7013802_1.fastq.gz | Fastqsanger.gz |
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Project description:Whole-transcriptome analysis and western blotting of sauchinone-treated HepG2 cells demonstrated that sauchinone regulated genes relevant to cholesterol metabolism and synthesis. In particular, it was found that the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9) was downregulated, and the expression of low density lipoprotein receptor (LDLR) was upregulated in sauchinone-treated HepG2 cells. Consequently, LDL-cholesterol (LDL-C) uptake was increased. As a transcriptional regulator of PCSK9 expression, sterol regulatory elements binding protein-2 (SREBP-2) was proposed by transcriptome analysis and western blotting. Oral administration of sauchinone increased hepatic LDLR through PCSK9 inhibition in obese mice and showed the reduced serum LDL-C levels and downstream targets of SREBP-2. Thus, it is evident that sauchinone reduces hepatic steatosis by downregulating the expression of hepatic PCSK9 via SREBP-2.
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