HSP90 pathway in intermediate mononuclear cells causes plaque erosion via induction of neutrophil hyper-responsiveness

Abstract Aim To explore the function(s) of HSP90 in intermediate monocyte-mediated plaque erosion. Materials and methods We used single-cell RNA sequencing to map cardiac immune response composition patients with rupture By focusing our analyses on CD14 positive monocytes, we obtained a higher resolution identification cell subsets experiencing erosion rupture. interpreted findings using gene ontology (GO) enrichment Kyoto Encyclopedia Genes Genomes (KEGG) databases by performing receiver operating characteristic (ROC) curve analysis. Results Single-cell analysis mononuclear cells peripheral blood five ACS confirmed that monocytes were main leading ACS. Interestingly, results suggested significant increase proportion atypical (C4 subsets) rupture, which was novel finding. This may be caused increased migration into during found monocyte activation most obvious (C1, C10, C11), C1 subgroup (FCGR3B/CMTM2 double strong positive; subsequently defined as monocytes) very high. further role erosion, GO KEGG pathway performed. indicated are highly involved neutrophil metabolism. Because neutrophils effector induce reasonably infer can all subtypes expressed monocytes. thus collected from (n=150) for transcriptomics intracellular proteomics ROC demonstrated area under HSP90-based prediction 0.86, indicating could predict if would experience Conclusion Activation expression crucial event induces hyper-responsiveness leads Funding Acknowledgement Type funding sources: Other. Main source(s): China,Shanghai Science Technology Commission