ArticleBalkan medical journal2025
Mechanism of Neutrophil p90RSK-Nrf2 Signaling Pathway in Atherosclerosis.
Article in Balkan medical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: MRP8/14, a calcium-binding protein of the S100 family, is predominantly expressed in myeloid cells and exhibits proinflammatory and prothrombotic properties. Platelet-neutrophil interactions can trigger MRP8/14 release, but their role in atherosclerosis (AS) remains unclear. Aims: To investigate the effect of MRP8/14 on AS progression and the underlying mechanisms involved, focusing on neutrophil activation and the toll-like receptor 4 (TLR4)-ERK1/2-p90RSK and NRF2-ARE pathways. Study Design: Ex vivo and animal study. Methods: Neutrophils isolated from mouse bone marrow were stimulated with P-selectin to induce MRP8/14 release, which was subsequently quantified using ELISA. Neutrophil extracellular traps (NET) formation was induced by phobolol 12-myristate 13-acetate, and Mrp8/14 expression was examined via fluorescence labeling. Cytokine release and CD11b expression were assessed using flow cytometry. An AS mouse model was established by administering a high-fat diet. Atherosclerotic plaque size was analyzed using Oil Red O staining. Proteins from the TLR4-ERK1/2-p90RSK and NRF2-ARE pathways were analyzed by Western blotting. Results: P-selectin induced MRP8/14 release, which was inhibited by P-selectin antagonists. NET formation also contributed to MRP8/14 secretion. hMRP8/14 treatment enhanced CD11b expression, neutrophil adhesion, and proinflammatory cytokine secretion. In AS mice, MRP8/14 secretion was linked to TLR4 upregulation, ERK1/2-p90RSK signaling activation, and NRF2-ARE pathway inhibition. Paquinimod, an MRP8/14 antagonist, mitigated neutrophil activation, inflammation, and arterial plaque formation. Conclusion: MRP8/14 secreted from neutrophils activates the ERK1/2-p90RSK pathway via TLR4 and suppresses the NRF2-ARE pathway, driving inflammation and promoting AS progression.
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