{"doi":"10.1101/2025.08.12.669996","title":"Increased atherosclerosis and expression of inflammarafts in macrophage foam cells in AIBP-deficient mice","abstract":"Background: Atherosclerotic lesions comprise different populations of macrophages, including lipid-laden macrophage foam cells and non-foamy, inflammatory macrophages, playing different roles in disease progression. Previous studies demonstrated higher expression of inflammarafts - enlarged, cholesterol-rich lipid rafts hosting assemblies of inflammatory receptors - in non-foamy, inflammatory macrophages, as opposed to lower inflammarafts in lipid-lade macrophage foam cells. Apolipoprotein A-I Binding Protein (AIBP) facilitates cholesterol efflux from macrophages and has been shown to reduce inflammatory responses and protect against atherosclerosis. This study investigated the effect of AIBP deficiency on inflammaraft expression in aortic foam cells and non-foamy macrophages in hypercholesterolemic mice. Methods: macrophages were gated for BODIPY-high foamy and BODIPY-low non-foamy cells and analyzed for the expression of inflammaraft markers TLR4 (toll-like receptor-4) dimers and lipid rafts. Consecutive sections of the aortic root were stained with modified Van Gieson stain to assess lesion and necrotic core sizes. Results: mice. Male and female mice showed similar results. Conclusions: Our results indicate that AIBP deficiency leads to the formation of a new foam cell phenotype in which the increased lipid accumulation is associated with an increased expression of TLR4 inflammarafts. This transition of foam cells to a proinflammatory phenotype correlates with the development of advanced atherosclerotic plaques.","journal":"bioRxiv (Cold Spring Harbor Laboratory)","year":2025,"id":558790,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9565,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2025-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1335598,"name":"Nicolaus Nazarenkov","orcid":null,"position":1,"is_corresponding":false},{"id":896222,"name":"Е. А. Алексеева","orcid":"0000-0002-9660-9042","position":2,"is_corresponding":false},{"id":636269,"name":"Juliana M. Navia‐Pelaez","orcid":"0000-0001-5709-339X","position":3,"is_corresponding":false},{"id":323767,"name":"Aakash Patel","orcid":"0000-0002-1846-8862","position":4,"is_corresponding":false},{"id":814862,"name":"Patrick Secrest","orcid":null,"position":5,"is_corresponding":false},{"id":106556,"name":"Philip L.S.M. Gordts","orcid":"0000-0001-7224-4328","position":6,"is_corresponding":false},{"id":246518,"name":"Sven Heinz","orcid":"0000-0002-4665-1007","position":7,"is_corresponding":false},{"id":264535,"name":"Yury I. Miller","orcid":"0000-0003-0521-7690","position":8,"is_corresponding":false},{"id":896221,"name":"Hui Li","orcid":"0009-0007-4155-0868","position":0,"is_corresponding":true}],"reference_count":18,"raw_metadata":null,"created_at":"2026-07-19T02:55:30.312295Z","pmid":"40832194","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}