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SMARCAL1 modulates cellular triglyceride storage and expenditure in response to cell growth states via interaction with ANGPTL3 (RNA-Seq 2)

ABSTRACT: SMARCAL1 modulates cellular triglyceride storage and expenditure in response to cell growth states via interaction with ANGPTL3 (RNA-Seq 2)

PROVIDER: PRJNA914048 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22822758_1.fastq.gz	Fastqsanger.gz
	SRR22822758_2.fastq.gz	Fastqsanger.gz
	SRR22822759_1.fastq.gz	Fastqsanger.gz
	SRR22822759_2.fastq.gz	Fastqsanger.gz
	SRR22822760_1.fastq.gz	Fastqsanger.gz

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SMARCAL1 modulates cellular triglyceride storage and expenditure in response to cell growth states via interaction with ANGPTL3 (RNA-Seq 2)

Project description:SMARCAL1 is a chromatin regulator. Biallelic mutations of SMARCAL1 cause Schimke Immunoosseous Dysplasia (SIOD), a disease with severe growth defects and premature death. Atherosclerosis and hyperlipidemia are common phenotypes among SIOD patients. However, little is known about their genesis and development. Here we show that SMARCAL1 is vital in regulating cellular lipid metabolism. Using a proteomic approach, we found that SmarcAL1 interacts with angiopoietin-like 3 (Angptl3), a key lipoprotein regulator. SmarcAL1 deficiency in cell models resulted in substantial accumulation of triglycerides (TGs) and fatty acids (FAs). SmarcAL1 KO in mice drastically increased plasma TG level. The nuclear SmarcAL1 translocates into cytoplasm, surprisingly, enriched at peroxisomes, where it interacts with Angptl3. This shuttling provides a regulatory control over cellular lipid metabolism via SmarcAL1-regulated gene expression, in response to cell growth states. Inactivation of SmarcAL1 gene reduced the expression of the genes responsible for FA metabolism, suggesting that SmarcAL1 plays a key role in regulating lipid metabolism. Indeed, the Angptl3-mediated TG partition is largely dependent on SmarcAL1 activity. This activity was further supported by two opposite SMARCAL1 single-tissue expression profiles linked to two quantitative trait loci that are differentially associated with body mass index. Thus, SMARCAL1 is crucial for cellular lipid metabolism, and ANGPTL3-regulated SMARCAL1 activities enable cells to response to cell growth states for TG storage or expenditure.

2024-01-02 | GSE221373 | GEO

Transcriptomic profile of ANGPTL3-deficient HepG2 cells

Project description:Cardiovascular disease is a leading cause of death worldwide, and inhibition of the hepatically secreted protein ANGPTL3 has emerged as an effective treatment for lowering low-density lipoprotein cholesterol (LDL), the cardinal risk factor for coronary artery disease (CAD). In this study, we examine the effects of complete genetic deficiency of ANGPTL3 on the hepatocyte transcriptome using a HepG2 cell culture model with the ANGPTL3 locus "knocked out" (KO) via CRISPR-Cas9.

2023-05-15 | GSE232045 | GEO

ANGPTL3 deficiency alters the lipid profile and metabolism of cultured hepatocytes and human lipoproteins

Project description:Even though the functions of ANGPTL3 in the circulation are relatively well characterized, many mechanistic questions regarding the molecular consequences of ANGPTL3 loss-of-function and protection against cardiovascular disease remain unanswered. To help understant the molecular mechanisms exerted by ANGPTL3 deficiency, we studied the alterations of ANGPTL3 loss-of-function in hepatocytes and plasma lipid molecular species profiles.

2023-04-06 | GSE229133 | GEO

The effect of ANGPTL3 mAb on liver transcriptomes in LDLR-deficient mice

Project description:Purpose: The goal of this study was to evaluate the effect of ANGPTL3 inhibition on liver transcriptomes in LDLR KO mice. Methods: Mice were treated once weekly for 3 weeks with 25mg/kg control mAb or ANGPTL3 mAb. Livers were harvested 6 days after the last mAb treatment. Results: ANGPTL3 inhibition had no major impact on hepatic gene expression.

2020-07-05 | GSE143726 | GEO

The Drosophila Estrogen-Related Receptor acts within the larval fat body to promote triglyceride storage

Project description:Members of the Estrogen-Related Receptor (ERR) family of nuclear receptors (NR) serve a key role in coordinating triglyceride (TAG) accumulation with juvenile growth and development. In both insects and mammals, loss of ERR activity disrupts (TAG) storage during the post-embryonic growth phase, with loss-of-function mutations in mouseErraandDrosophila melanogaster dERRinducing a lean phenotype. However, the role of insect ERRs in controlling TAG accumulation remains poorly understood, as previous multiomic studies largely relied on whole animal analyses. Here we address this shortcoming by using tissue-specific approaches to determine how dERR regulates lipid metabolism within theDrosophilalarval fat body. We found that dERR autonomously promotes TAG accumulation within fat body cells by regulating expression of genes involved in glycolysis, the pentose phosphate pathway, lipid synthesis, andb-oxidation. As an extension of these results, we not only discovered thatdERRmutant fat bodies exhibit decreased expression of known HNF4 target genes but also found that dHNF4 activity is decreased indERRmutants. Overall, our findings indicate that dERR plays a multifaceted role in the larval fat body to coordinate lipid storage with developmental growth and hint at a conserved mechanism by which ERR and HNF4 homologs coordinately regulate metabolic gene expression

2024-08-02 | GSE273774 | GEO

Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression

Project description:This SuperSeries is composed of the following subset Series: GSE35551: Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (1) GSE35552: Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (2) GSE35553: Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (3) Refer to individual Series

2012-04-04 | E-GEOD-35554 | biostudies-arrayexpress

The Drosophila Estrogen-Related Receptor acts within the larval fat body to promote triglyceride storage

Project description:The Drosophila Estrogen-Related Receptor acts within the larval fat body to promote triglyceride storage

| PRJNA1143037 | ENA

Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (3)

Project description:Biallelic mutations of the DNA annealing helicase SMARCAL1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin, subfamily a-like 1) cause Schimke immuno-osseous dysplasia (SIOD, MIM 242900), an incompletely penetrant autosomal recessive disorder. Using human, Drosophila, and mouse models, we show that the proteins encoded by SMARCAL1 orthologues localize to transcriptionally active chromatin and modulate gene expression. We also show that similar to SIOD patients, deficiency of the SMARCAL1 orthologues alone is insufficient to cause disease in fruit flies and mice although such deficiency causes modest diffuse alterations in gene expression. Rather, disease manifests when SMARCAL1 deficiency interacts with genetic and environmental factors that further alter gene expression. We conclude that the SMARCAL1 annealing helicase buffers fluctuations in gene expression and that alterations in gene expression contribute to the penetrance of SIOD.

2012-04-05 | GSE35553 | GEO

Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (2)

2012-04-05 | GSE35552 | GEO

Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (1)

2012-04-05 | GSE35551 | GEO