Fig 1: Plasma SERPINA3 levels elevated in different groups. (A) Comparison of plasma SERPINA3 levels in patients with CAD and non-CAD. (B) Comparison of plasma SERPINA3 levels in patients with non-CAD, stable CAD, and ACS. (C) Stratified analysis was performed by the number of diseased vessels. (D) Association between log-transformed plasma SERPINA3 levels and Syntax II score. (E) Receiver operating characteristic (ROC) curves confirmed that plasma SERPINA3 levels significantly differentiated CAD patients. Area under the curve (AUC) = 0.64, 95% CI:0.55–0.73, P = 0.004 for the significant AUC. *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 2: Associations between log-transformed plasma SERPINA3 levels and inflammation-related parameters. Associations between log-transformed plasma SERPINA3 levels and WBC counts (A), CRP (B), neutrophils (C), lymphocytes (D), and NLR (E). WBC, white blood cell; CRP, C-reactive protein; NLR, neutrophils to lymphocytes ratio.
Fig 3: Secreted SERPINA3 regulated the release of inflammatory factors in HUVECs. (A) HUVECs were treated with SERPINA3 (100 ng/mL) and ox-LDL (100 µg/mL) for 18 h, cells proliferation in different groups was determined by EdU assay. (B) Quantification of RASMCs proliferation rates. Data are mean ± SD. n = 3 independent experiments, two-way ANOVA with Bonferroni post-test, ns = 0.05, *P < 0.05, **P < 0.01. (C) HUVECs migration in different groups was determined by scratch assays at 0 and 12 h after wounding. (D) Quantification of RASMCs wound closure index, namely the distance migrated at time 0 relative to the distance at 12 h. Data are mean ± SD. n = 3 independent experiments, two-way ANOVA with Bonferroni post-test, ns = 0.05, ***P < 0.005, ****P < 0.001. (E–I) qPCR was performed for PCNA, CCND1, IL-6, MCP-1, and ICAM of HUVECs in different groups. Data are mean ± SD. n = 3 independent experiments, two-way ANOVA with Bonferroni post-test, ns = 0.05, *P < 0.05, **P < 0.01, ****P < 0.001.
Fig 4: ELISA-based biomarker validation. Levels of seven candidate biomarkers were determined in the whole plasma of CCA (n = 26), normal controls (n = 20), and disease control (DC; n = 17). AACT, alpha-1-antichymotrypsin; AFM, afamin; AMBP, alpha-1 microglobulin; NGAL, neutrophil gelatinase-associated lipocalin; PSMA3, proteasome subunit alpha type-3; TAOK3, TAO kinase 3.
Fig 5: SERPINA3 activated proliferation and migration by NF-?B in RASMCs. (A) RASMCs was transferred SERPINA3 siRNA for 36 h and stimulated by ox-LDL for 12 h, protein expression of p65, t-I?Ba, p- I?Ba, PCNA, CCND1, and vinculin were measured by western blot. (B–E) Quantification of relative protein level of p65, p- I?Ba, PCNA, CCND1 in (A). Data are mean ± SD. n = 3 independent experiments, two-way ANOVA with Bonferroni post-test, ns = 0.05, *P < 0.05, **P < 0.01, ****P < 0.001. (F–I) qPCR was performed for PCNA, CCND1, IL-6, and MCP-1 of RASMCs in different groups. Data are mean ± SD. n = 3 independent experiments, two-way ANOVA with Bonferroni post-test, ns = 0.05, *P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.001.
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