Additional file 2 of Platelets in preeclampsia: an observational study of indices associated with aspirin nonresponsiveness, activation and transcriptional landscape

Additional file 2. Figure S1. Participant selection flowchart. Figure S2. The expression and colocalization of CD42b and CD62P in placental villous and decidual tissues. FI: fluorescence intensity, ASA: aspirin, PE: preeclampsia, nPE: nonpreeclampsia, MC: Mander’s coefficient, PCC: Pearson’s coefficient, **p < 0.01, ns: nonsignificant. Figure S3. Gene Ontology (GO) analysis of differentially expressed mRNAs in platelets obtained from blood, placental villous and decidua in the HR-PE vs HR-nPE groups. The top 15 enriched GO terms in the biological process (BP), cellular component (CC), and molecular function (MF) categories. The colour and size of the circle represent the q value and gene count, respectively. Figure S4. Enrichment plots in blood, placental villous and decidua using GSEA. NES: normalised enrichment score, HR: high risk, PE: preeclampsia, nPE: nonpreeclampsia. Table S1. Primers used in the RT‒qPCR experiment. Table S2. Demographic and clinical characteristics of the study participants in Opal immunofluorescence staining. Table S3. Demographic and clinical characteristics of the study participants in RNA-seq. Table S4. Demographic and clinical characteristics of the study participants in the RT‒qPCR validation. Table S5. Linear mixed-effects models for PC, MPV and PC/MPV: fixed effects. Table S6. Pairwise comparisons of platelet indices across gestation. Table S7. Screening performance of platelet indices and maternal factors for aspirin nonresponsiveness. Table S8. The quality control metrics and alignment results for the RNA-seq data. Table S9. Gene sets upregulated in the high-risk aspirin-treated with preeclampsia (HR-PE) group. Table S10. Gene sets upregulated in the high-risk aspirin-treated without preeclampsia (HR-nPE) group

附加文件2。图S1：研究对象筛选流程图。图S2：胎盘绒毛与蜕膜组织中CD42b和CD62P的表达及共定位情况。注：FI为荧光强度（fluorescence intensity），ASA为阿司匹林（aspirin），PE为子痫前期（preeclampsia），nPE为非子痫前期（nonpreeclampsia），MC为曼德系数（Mander’s coefficient），PCC为皮尔逊相关系数（Pearson’s coefficient），**p < 0.01**表示极显著差异，ns表示无统计学意义（nonsignificant）。图S3：高风险子痫前期（HR-PE）组与高风险非子痫前期（HR-nPE）组受试者血液、胎盘绒毛及蜕膜来源血小板中差异表达mRNA的基因本体（Gene Ontology, GO）富集分析，展示了生物过程（biological process, BP）、细胞组分（cellular component, CC）及分子功能（molecular function, MF）三个分类下富集度排名前15的GO条目，圆点的颜色与大小分别代表校正后P值（q value）与富集基因数。图S4：采用基因集富集分析（Gene Set Enrichment Analysis, GSEA）对血液、胎盘绒毛及蜕膜组织进行富集分析得到的结果图。注：NES为标准化富集得分（normalised enrichment score），HR为高风险（high risk），PE为子痫前期（preeclampsia），nPE为非子痫前期（nonpreeclampsia）。表S1：逆转录实时定量聚合酶链反应（RT‒qPCR）实验所用引物。表S2：Opal免疫荧光染色实验中研究对象的人口学与临床特征。表S3：RNA测序（RNA-seq）实验中研究对象的人口学与临床特征。表S4：RT‒qPCR验证实验中研究对象的人口学与临床特征。表S5：血小板计数（PC）、平均血小板体积（MPV）及PC/MPV比值的线性混合效应模型固定效应分析结果。表S6：妊娠各阶段血小板相关指标的两两比较结果。表S7：血小板相关指标与母体因素对阿司匹林无应答的筛查性能评估结果。表S8：RNA-seq数据的质量控制指标与比对结果。表S9：高风险阿司匹林治疗并发子痫前期（HR-PE）组上调的基因集。表S10：高风险阿司匹林治疗未并发子痫前期（HR-nPE）组上调的基因集