Fig. 5

Effects of ADSCs treatment on CLP-induced coagulation dysfunction. GO analysis was performed to define biological processes enriched by DEGs between the CLP + ADSCs4 versus CLP + Vehicle groups (A). WGCNA was performed based on the 1215 ADSCs-responsive DEGs in PBMCs. Correlations between module eigengenes and different doses of ADSCs treatment were considered to be significant based on the criteria (correlation coefficients > 0.5 or < -0.5 and p value < 0.05) (B). The expression patterns of hub genes (|MM|> 0.8 and |GS|> 0.35) in the turquoise, brown and green modules were visualized by heatmap (C). GO analysis was performed to identify the annotated terms enriched for hub genes in each module, and the number of enriched genes was labeled on the corresponding GO term (D). Protein–protein interaction (PPI) network analysis was carried out to identify key driver (KD) genes responsible for the induction or inhibition of the coagulation pathway in PBMCs in the turquoise and green modules, respectively (E). Validation of the expression patterns of Itgb3 and F5 in PBMCs by RT-qPCR analysis. n = 4 in each group. *, p < 0.05, significantly different from the CLP + Vehicle group (F). Coagulation assays were performed to examine changes in plasma prothrombin time (PT) and activated partial thromboplastin time (APTT) at 6 h after vehicle or ADSCs treatment in CLP mice. Sham-operated mice served as controls. n = 5–7. *, p < 0.05 (G). Representative images demonstrating differences in fibrin deposition in the pulmonary vasculature in different treatment groups; fibrin deposition: blue arrow. Images were taken by Nikon 80i microscopy and SPOT Software at a resolution of 96 dpi, and processed in Adobe Photoshop at a resolution of 600 dpi. No downstream processing was utilized. Scar bar = 100 μm (H). Quantification of the number of thrombi observed per field in different groups. n = 3–6. *, p < 0.05 (I)