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Macrophage programming is regulated by a cooperative interaction between fatty acid binding protein 5 and peroxisome proliferator-activated receptor gamma

ABSTRACT: Macrophage programming is regulated by a cooperative interaction between fatty acid binding protein 5 and peroxisome proliferator-activated receptor gamma

PROVIDER: PRJNA797465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17624272_1.fastq.gz	Fastqsanger.gz
	SRR17624272_2.fastq.gz	Fastqsanger.gz
	SRR17624273_1.fastq.gz	Fastqsanger.gz
	SRR17624273_2.fastq.gz	Fastqsanger.gz
	SRR17624274_1.fastq.gz	Fastqsanger.gz

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Macrophage programming is regulated by a cooperative interaction between fatty acid binding protein 5 and peroxisome proliferator-activated receptor gamma

Project description:The resolution of inflammation is an active process that is tightly regulated to achieve repair and tissue homeostasis. In the absence of resolution, chronic inflammation underlies the pathogenesis of chronic lung disease including Chronic Obstructive Pulmonary Disease (COPD) with recurrent exacerbations. Over the course of inflammation, macrophage programming transitions from inflammatory to pro-resolving, and is in part regulated by the nuclear receptor Peroxisome Proliferator-Activated Receptor γ (PPARγ). In our previous work, we demonstrated an association between Fatty Acid Binding Protein 5 (FABP5) expression and PPARg activity in PBMCs. However, the role of FABP5 in macrophage programming is not yet defined, thus, we further investigated its interaction with PPARγ and its role in macrophage programming. Here, we demonstrate that FABP5 is necessary to initiate PPARγ activation and macrophage pro-resolving programming. We used the RNAscope tool in combination with co-immunofluorescence, immunoprecipitation, PPARγ activity assay, and chromatin immunoprecipitation to show that FABP5 and PPARγ not only interact but also regulate one another. By integrating flow cytometry, ELISA, assay for transposase-accessible chromatin by sequencing (ATAC-seq) and the Seahorse technology, we extend our findings to illustrate that lack of FABP5 expression promotes a glycolytic pro-inflammatory macrophage programming. Taken together, these data provide evidence that FABP5 and PPARγ reciprocally regulate each other’s expression and function, consistent with a positive feedback regulatory loop between the two to promote macrophage pro-resolving programming.

2023-12-08 | GSE193748 | GEO

Macrophage programming is regulated by a cooperative interaction between fatty acid binding protein 5 and peroxisome proliferator-activated receptor γ.

Project description:Resolution of inflammation is an active process that is tightly regulated to achieve repair and tissue homeostasis. In the absence of resolution, persistent inflammation underlies the pathogenesis of chronic lung disease such as chronic obstructive pulmonary disease (COPD) with recurrent exacerbations. Over the course of inflammation, macrophage programming transitions from pro-inflammatory to pro-resolving, which is in part regulated by the nuclear receptor Peroxisome Proliferator-Activated Receptor γ (PPARγ). Our previous work demonstrated an association between Fatty Acid Binding Protein 5 (FABP5) expression and PPARγ activity in peripheral blood mononuclear cells of healthy and COPD patients. However, a role for FABP5 in macrophage programming has not been examined. Here, using a combination of in vitro and in vivo approaches, we demonstrate that FABP5 is necessary for PPARγ activation. In turn, PPARγ acts directly to increase FABP5 expression in primary human alveolar macrophages. We further illustrate that lack of FABP5 expression promotes a pro-inflammatory macrophage programming with increased secretion of pro-inflammatory cytokines and increased chromatin accessibility for pro-inflammatory transcription factors (e.g., NF-κB and MAPK). And finally, real-time cell metabolic analysis using the Seahorse technology shows an inhibition of oxidative phosphorylation in FABP5-deficient macrophages. Taken together, our data indicate that FABP5 and PPARγ reciprocally regulate each other's expression and function, consistent with a novel positive feedback loop between the two factors that mediates macrophage pro-resolving programming. Our studies highlight the importance of defining targets and regulatory mechanisms that control the resolution of inflammation and may serve to inform novel interventional strategies directed towards COPD.

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