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ZFP36L1 Regulates Fgf21 mRNA Turnover and Modulates Alcoholic Hepatic Steatosis and Inflammation in Mice

ABSTRACT: ZFP36L1 Regulates Fgf21 mRNA Turnover and Modulates Alcoholic Hepatic Steatosis and Inflammation in Mice

PROVIDER: PRJNA686111 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13268656_1.fastq.gz	Fastqsanger.gz
	SRR13268656_2.fastq.gz	Fastqsanger.gz
	SRR13268657_1.fastq.gz	Fastqsanger.gz
	SRR13268657_2.fastq.gz	Fastqsanger.gz
	SRR13268658_1.fastq.gz	Fastqsanger.gz

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ZFP36L1 Regulates Fgf21 mRNA Turnover and Modulates Alcoholic Hepatic Steatosis and Inflammation in Mice

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ZFP36L1

Project description:ZFP36L1

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FGF21 treatment and iPSC-derived neurons

Project description:FGF21 analogs tested in clinical trials in metabolic diseases i.e. type 2 diabetes mellitus and non-alcoholic fatty liver disease are generally well-tolerated. FGF21 is a peptide hormone that is primarily secreted by the liver, but it also crosses the blood-brain barrier. The bulk of literature on this subject has raised the possibility that FGF21 administration could affect alcohol use and reward behaviors. Our recent study showed that FGF21 levels were associated with recent alcohol consumption. Furthermore, our data also suggest that the effects of FGF21 in the induced pluripotent stem cell (iPSC)-derived 3D-brain organoids are associated, at least in part, with the regulation of catecholamines, neurotransmitters that play a crucial role in reward pathways. These observations potentially open the way to pharmacologic manipulation of FGF21, which in turn could have significant implications for catecholamines, and alcohol use. Current in vitro models designed to study drug action in the human brain are limited. Therefore, we used iPSC-derived neurons as a novel "cell-line based" approach to advance our understanding of drug action in the brain. Since the half-life of the naïve form of FGF21 is about 0.5-2 hours, it is not suitable for clinical use due to poor pharmacokinetic and biophysical properties . As a result, the present study was designed to identify molecular mechanisms for both the naïve form of FGF21 and a long-acting FGF21 molecule (PF-05231023) which was developed by conjugating two molecules of modified FGF21 (dHis/Ala129Cys) to an antibody scaffold.

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Project description:Fibroblast growth factor 21 (Fgf21) is a liver-derived, fasting-induced hormone with broad effects on growth, nutrient metabolism and insulin sensitivity. Here, we report the discovery of a novel mechanism regulating Fgf21 expression under growth and fasting-feeding. The Sel1LHrd1 complex is the most conserved branch of mammalian endoplasmic reticulum (ER)- associated degradation (ERAD) machinery. Mice with liver-specific deletion of Sel1L exhibit growth retardation with markedly elevated circulating Fgf21, reaching levels close to those in Fgf21 transgenic mice or pharmacological models. Mechanistically, we show that the Sel1LHrd1 ERAD complex controls Fgf21 transcription by regulating the ubiquitination and turnover (and thus nuclear abundance) of ER-resident transcription factor Crebh, while having no effect on the other well-known Fgf21 transcription factor Pparα. Our data reveal a physiologically regulated, inverse correlation between Sel1L-Hrd1 ERAD and Crebh-Fgf21 levels under fasting-feeding and growth. This study not only establishes the importance of Sel1L-Hrd1 ERAD in the liver in the regulation of systemic energy metabolism, but also reveals a novel hepatic “ERADCrebh- Fgf21” axis directly linking ER protein turnover to gene transcription and systemic metabolic regulation.

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