A BAFF/APRIL axis regulates obesogenic-diet driven weight gain
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA543147 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9066690.fastq.gz | Fastqsanger.gz | |||
| SRR9066691.fastq.gz | Fastqsanger.gz | |||
| SRR9066692.fastq.gz | Fastqsanger.gz | |||
| SRR9066693.fastq.gz | Fastqsanger.gz | |||
| SRR9066694.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: To define the role of the BAFF/APRIL axis in the regulation of adipose tissue homeostasis through RNAseq. Methods: Primary adipocytes were derived from pre-adipocyte precursors of inguinal white adipose from male C57BL/6 mice aged 6-8 weeks. Adipocytes were treated with rBAFF, rAPRIL, or multiple controls for 24 hours. mRNA profiles were generated for each condition, run in biological duplicates, using Illumina HiSeq2000 with single-end, 50bp reads. Differential gene lists were generated by comparing BAFF and APRIL to controls using unpaired ttests. Results:Following mapping an average of 30million reads across 10 samples to the mm10 mouse genome with annotations from UCSC, differential analysis identified genes involved in adipocyte pathways associated with lipid metabolism, lipolysis, and inflammation. Conclusion: BAFF and APRIL modulate modulate white adipocyte lipid handling.
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Project description:Emerging clinical evidence points to a function for B cell activating factor (BAFF) in pregnancy. However, a direct role for BAFF-axis members including BAFF, the closely related a proliferation-inducing ligand (APRIL), and their respective receptors in pregnancy has not been examined. This study demonstrates that loss of BAFF results in decreased inflammatory responsiveness and decreased susceptibility to inflammation-induced preterm birth (PTB). In contrast, loss of APRIL increases inflammatory responsiveness and susceptibility to PTB. Consistent with overlapping receptor utilization by BAFF and APRIL, deletion of BAFF-axis receptors is not sufficient to modify susceptibility to PTB. Critically, therapeutic administration of BAFF/APRIL monoclonal antibodies or recombinant proteins is sufficient to manipulate susceptibility to inflammation-induced PTB. Further, macrophages are identified as the principle BAFF producing immune cells at the maternal-fetal interface and BAFF and APRIL divergently manipulate macrophage gene expression and inflammatory function. Genes linked to labor initiation are upregulated in WT and APRIL deficient macrophages while downregulated in BAFF deficient macrophages and correlate with myeloid gene expression in human placental samples during labor. Thus, BAFF and APRIL play important, but divergent, counterregulatory inflammatory roles in pregnancy and provide new therapeutic targets for mitigating the risk of PTB.
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Project description:The impact of immune mediators on weight homeostasis remains underdefined. Interrogation of resistance to diet-induced obesity in mice lacking a negative regulator of Toll-like receptor signaling serendipitously uncovered a role for B cell activating factor (BAFF). Here we show that overexpression of BAFF in multiple mouse models associates with protection from weight gain, approximating a log-linear dose response relation to BAFF concentrations. Gene expression analysis of BAFF-stimulated subcutaneous white adipocytes unveils upregulation of lipid metabolism pathways, with BAFF inducing white adipose tissue (WAT) lipolysis. Brown adipose tissue (BAT) from BAFF-overexpressing mice exhibits increased Ucp1 expression and BAFF promotes brown adipocyte respiration and in vivo energy expenditure. A proliferation-inducing ligand (APRIL), a BAFF homolog, similarly modulates WAT and BAT lipid handling. Genetic deletion of both BAFF and APRIL augments diet-induced obesity. Lastly, BAFF/APRIL effects are conserved in human adipocytes and higher BAFF/APRIL levels correlate with greater BMI decrease after bariatric surgery. Together, the BAFF/APRIL axis is a multifaceted immune regulator of weight gain and adipose tissue function.
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2024-11-14 | GSE236579 | GEO
Project description:Reducing body weight to improve metabolic health and related comorbidities is a primary goal in treating obesity. However, maintaining weight loss is a considerable challenge, especially as the body appears to retain an obesogenic memory that defends against body weight changes. Overcoming this barrier for long-term treatment success is difficult because the molecular mechanisms underpinning this phenomenon remain largely unknown. Here, by using single-nuclei RNA-sequencing, we show that both human and mouse adipose tissue retain cellular transcriptional changes after appreciable weight loss. Furthermore, we find persistent obesity-induced alterations in the mouse adipocyte epigenome, negatively affecting their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain, and the epigenetic memory can explain future transcriptional deregulation in adipocytes in response to further high-fat diet feeding. In summary, our findings indicate the existence of an obesogenic memory, largely based on stable epigenetic changes, in mouse adipocytes, and likely other cell types. These changes appear to prime cells for pathological responses in an obesogenic environment, contributing to the problematic "yo-yo" effect often seen with dieting. Targeting these changes in the future could improve long-term weight management and health outcomes.
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