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Lipolysis-derived linoleic acid drives beige fat progenitor cell proliferation via CD36

ABSTRACT: Lipolysis-derived linoleic acid drives beige fat progenitor cell proliferation via CD36

PROVIDER: PRJNA833660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19018938_1.fastq.gz	Fastqsanger.gz
	SRR19018938_2.fastq.gz	Fastqsanger.gz
	SRR19018939_1.fastq.gz	Fastqsanger.gz
	SRR19018939_2.fastq.gz	Fastqsanger.gz
	SRR19018940_1.fastq.gz	Fastqsanger.gz

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Lipolysis-derived linoleic acid drives beige fat progenitor cell proliferation via CD36

Project description:To investigate what stimulates beige progenitor cell proliferation, we performed RNA-seq of primary isolated CD81+ cells (Lin-: Sca1+: CD81+) and CD81- cells (Lin-: Sca1+: CD81-) in the inguinal WAT of mice.

2022-11-04 | GSE201930 | GEO

Lipolysis Engages CD36 to Promote ZBP1-Mediated Necrosis Impairing Lung Regeneration in COPD

Project description:Lung parenchyma destruction represents a severe condition commonly found in chronic obstructive pulmonary disease (COPD), the leading cause of morbidity and mortality worldwide. Promoting lung regeneration is crucial for achieving clinical improvement. However, no therapeutic drugs are approved to improve the regeneration capacity due to incomplete understanding of the underlying pathogenic mechanisms. Here, we identify a positive feedback loop formed between adipose triglyceride lipase (ATGL)-mediated lipolysis and overexpression of CD36 specific to lung epithelial cells, contributing to disease progression. Genetic deletion of CD36 in lung epithelial cells and pharmacological inhibition of either ATGL or CD36 effectively reduce COPD pathogenesis and promote lung regeneration in mice. Mechanistically, disruption of the ATGL-CD36 loop rescued Z-DNA binding protein 1 (ZBP1)-induced cell necroptosis and restored WNT/β-catenin signaling. Thus, we uncover a previously unrecognized crosstalk between lipolysis and lung epithelial cells, suggesting the regenerative potential for therapeutic intervention by targeting the ATGL-CD36-ZBP1 axis in COPD.

2024-12-13 | GSE246501 | GEO

TZD-induced beige fat activation

Project description:Beige fat cells dissipate energy through mitochondrial uncoupling protein UCP1 defending against obesity and can be activated by thermogenic stimuli in white adipose tissue. Here, we provide candidate molecules involved in beige fat activation induced the TZD, rosiglitazone.

2016-10-03 | GSE79031 | GEO

Lipolysis Engages CD36 to Promote ZBP1-Mediated Necrosis Impairing Lung Regeneration in COPD

Project description:Lipolysis Engages CD36 to Promote ZBP1-Mediated Necrosis Impairing Lung Regeneration in COPD

| PRJNA1033370 | ENA

CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells

Project description:Obesity-related muscular dysfunction and relative muscle atrophy affect an increasing number of people. Elucidating the molecular mechanisms of skeletal muscle cell development and growth may contribute to the maintenance of skeletal muscle mass in obesity. Fatty acid translocase (FAT/CD36), as a long-chain fatty acid transport protein, is crucial for lipid metabolism and signaling. CD36 is known to function in myogenic differentiation, and whether it affects the proliferation of skeletal muscle cells and the underlying mechanisms remain unclear. In this study, the effect of CD36 deficiency on skeletal muscle cell viability and proliferation was examined using C2C12 myoblasts. Results showed that the deletion of CD36 enhanced the inhibitory effect of PA on the proliferation and the promotion of apoptosis in skeletal muscle cells. Intriguingly, the silencing of CD36 suppressed cell proliferation by preventing the cell cycle from the G0/G1 phase to the S phase in a cyclin D1/CDK4-dependent manner. Overall, we demonstrated that CD36 was involved in skeletal muscle cell proliferation by cell cycle control, and these findings might facilitate the treatment of obesity-related muscle wasting.

2022-05-27 | GSE204686 | GEO

AMSC CD36+ subpopulations

Project description:AMSC CD36+ subpopulations

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Analysis of Wild Type and hepatocyte-specific CD36 knockout (CD36LKO) mice liver Transcriptomes under high fat diet (HFD)

Project description:We generated hepatocyte-specific CD36 knockout (CD36LKO) mice to study in vivo effects of CD36 on de novo lipogenesis (DNL) under high fat diet (HFD). Lipid deposition and DNL were analyzed in primary hepatocytes isolated from CD36LKO mice or HepG2 cells with CD36 overexpression. RNA-sequence, co-immunoprecipitation and proximity ligation assay were carried out to determine its role in regulating DNL. Results: Hepatic CD36 expression was upregulated in NAFLD mice and patients, and CD36LKO mice exhibited attenuated HFD-induced hepatic steatosis and insulin resistance. We identified hepatocyte CD36 as a key regulator for DNL in the liver. Sterol regulatory element-binding protein 1 (SREBP1) and its downstream lipogenic enzymes such as FASN, ACCα and ACLY were significantly downregulated in the liver of HFD-fed CD36LKO mice, whereas overexpression CD36 stimulated insulin-mediated DNL and lipid droplet formation in vitro. Mechanistically, CD36 was activated by insulin and formed a complex with insulin induced gene-2 (INSIG2), that disrupts the interaction between SREBP cleavage-activating protein (SCAP) and INSIG2, thereby leading to the translocation of SREBP1 from ER to Golgi for processing. Furthermore, treatment with 25-hydroxycholesterol or betulin, molecules shown to enhance SCAP/INSIG interaction, reversed the effects of CD36 on SREBP1 cleavage.

2022-01-03 | GSE191059 | GEO

AMSC CD36+ subpopulations

Project description:Adipose-derived MSCs (AMSC) are currently utilized in clinical trials for various diseases including osteoarthritis, amyotrophic lateral sclerosis, and multiple system atrophy. Whilst AMSCs may be defined by the surface expression of classical markers including CD44, CD90, CD105, and absence of CD45, these cells may exhbit donor-to-donor differences in differentiation potential. In this study we evaluated the expression of CD36 amongst AMSCs and utilized magnetic cell sorting to enrich for CD36+ cells. Whole transcriptome RNA-sequencing was performed on unsorted, CD36+ enriched, and CD36+ depleted cells to determine gene expression difference between these populations of cells. CD36 sorted or unsorted cells were then plated and maintained in growth medium. Cells were expanded for 2 passages and passage 8 cells were plated for RNA-sequencing analysis. Trizol reagent was used to harvest cells when they were proliferating cells (~80%) or 100% confluent cells.

2021-11-28 | GSE189525 | GEO

Age effects on CL-induced beige fat remodeling

Project description:Age effects on CL-induced beige fat remodeling

| PRJNA530012 | ENA

Beige Fat, Energy, and the Natriuretic Peptide System

Project description:Beige Fat, Energy, and the Natriuretic Peptide System

| PRJNA1065008 | ENA