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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-derived linoleic acid drives beige fat progenitor cell proliferation.

Project description:De novo beige adipocyte biogenesis involves the proliferation of progenitor cells in white adipose tissue (WAT); however, what regulates this process remains unclear. Here, we report that in mouse models but also in human tissues, WAT lipolysis-derived linoleic acid triggers beige progenitor cell proliferation following cold acclimation, β3-adrenoceptor activation, and burn injury. A subset of adipocyte progenitors, as marked by cell surface markers PDGFRα or Sca1 and CD81, harbored cristae-rich mitochondria and actively imported linoleic acid via a fatty acid transporter CD36. Linoleic acid not only was oxidized as fuel in the mitochondria but also was utilized for the synthesis of arachidonic acid-derived signaling entities such as prostaglandin D2. Oral supplementation of linoleic acid was sufficient to stimulate beige progenitor cell proliferation, even under thermoneutral conditions, in a CD36-dependent manner. Together, this study provides mechanistic insights into how diverse pathophysiological stimuli, such as cold and burn injury, promote de novo beige fat biogenesis.

| S-EPMC9875052 | biostudies-literature

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

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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

CD36

Project description:Monodelphis domestica CD36, CD36 molecule [Source:NCBI gene;Acc:100012876], is expressed in 1 baseline experiment(s);

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Project description:Anas platyrhynchos CD36, CD36 molecule [Source:HGNC Symbol;Acc:HGNC:1663], is differentially expressed in 1 experiment(s);

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Project description:Homo sapiens CD36, CD36 molecule [Source:HGNC Symbol;Acc:HGNC:1663], is differentially expressed in 134 experiment(s);

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Project description:Mus musculus Cd36, CD36 molecule [Source:MGI Symbol;Acc:MGI:107899], is differentially expressed in 138 experiment(s);