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Genetic ablation of myeloid integrin α9 attenuates early atherosclerosis
Journal article   Open access   Peer reviewed

Genetic ablation of myeloid integrin α9 attenuates early atherosclerosis

Tarun Barbhuyan, Rakesh B Patel, Ivan Budnik and Anil K Chauhan
Journal of leukocyte biology, Vol.116(5), pp.1208-1214
11/04/2024
DOI: 10.1093/jleuko/qiae161
PMCID: PMC11531806
PMID: 39036986
Appears in  UI Libraries Support Open Access
url
https://doi.org/10.1093/jleuko/qiae161View
Published (Version of record) Open Access

Abstract

Integrin α9β1 is known to stabilize leukocyte adhesion to the activated endothelium. We determined the role of myeloid cell α9β1 in early atherosclerosis in two models: α9MyeKOApoe−/− or the Ldlr−/− mice transplanted with bone marrow (BM) from α9Mye-KO mice fed a high-fat “Western” diet for four weeks. α9Mye-KOApoe−/− mice exhibited reduced early lesions in the aortae and aortic sinuses (p<0.05 vs. α9WT Apoe−/− mice). Similar results were obtained in α9Mye-KO BM→Ldlr−/− mice (p<0.05 vs α9WT BM→Ldlr−/− mice). Reduced early atherosclerosis in α9Mye-KOApoe−/− mice was associated with decreased neutrophil and neutrophil extracellular traps (NETs) content in the aortic lesions (p<0.05 vs. α9WTApoe−/−). VCAM-1-stimulated neutrophils from α9Mye-KO mice exhibited reduced adhesion, transmigration, and NETs formation (NETosis) (p<0.05 vs. α9WT neutrophils). Reduced NETosis was associated with decreased ERK phosphorylation, PAD4, and H3Cit expression. In summary, genetic ablation of myeloid cell-specific α9 reduces early atherosclerosis, most likely by reducing neutrophil adhesion, transmigration, and NETosis.
 atherosclerosis integrin α9β1 neutrophil extracellular traps neutrophils UIOWA OA Agreement

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