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A BAFF/APRIL axis regulates obesogenic-diet driven weight gain

ABSTRACT: A BAFF/APRIL axis regulates obesogenic-diet driven weight gain

PROVIDER: PRJNA543147 | ENA |

REPOSITORIES: ENA

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			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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A BAFF/APRIL axis regulates obesogenic-diet driven weight gain

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.

2021-02-08 | GSE131298 | GEO

BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

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:Antipsychotic drugs (APs) are used to treat psychiatric disorders but also have the prominent side effect of weight gain resulting in a higher incidence of metabolic disease in this patient group. While the majority of patients gain significant weight in response to APs some patients are relatively resistant to these effects. APs such as clozapine and olanzapine are deemed to be highly efficacious at treating psychiatric conditions yet they have some of the highest weight gain liabilities. Therefore, there is a need to determine which patients are less susceptible to the metabolic side effects of APs and would be good candidates for drugs such as olanzapine, and conversely, identifying patients that should be prescribed alternative APs with less weight gain liabilities.

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