Fig 2: pMSCs demonstrate differential expression of genes involved in coagulation and thrombosis: Real‐time PCR analysis (RT‐PCR) analysis of pro‐ and anti‐thrombotic genes expressed in pMSCs in comparison to HUVECs. (A) Genes inhibiting thrombosis and coagulation. TFPAI (Tissue Factor Pathway Inhibitor), PROC1 (Vitamin K‐dependent protein C1), PROS1 (Protein S1), SERPINC1 (Serpin Family C Member 1) and THBS4 (Thrombospondin 4). (B) Genes promoting thrombosis and coagulation. vWF (Von Willebrand Factor), GP6 (Glycoprotein VI platelet), PLCG2 (Phospholipase C Gamma 2), GRK5 (G Protein‐Coupled Receptor Kinase 5) and PLEK (Pleckstrin). Three independent experiments were performed for each cell type isolated from three different placentae. The data are expressed as fold change difference calculated from the ΔΔ−2 values. Bars represent mean ± SE. *p ≤ 0.05

Fig 3: (A) Western blot analysis of Bar-III on recombinant vWF-A1 domain (rvWF-A1). vWF-A1 (5 µg) was treated with Bar-III (4 µg) for 60 min at 37 °C, as described in methodology section. The proteolysis of vWF-A1 (indicated by an arrow) was analyzed using SDS-PAGE (7–15% gradient gel) and blotted with mice anti-vWF IgG. (B) Bar-III does not cleave the vWF receptor partner GPIbα on platelets. Washed platelets were incubated with Bar-III (4 µg) at 37 °C at the indicated intervals, and the reactions were terminated by addition of SDS loading sample buffer. The platelet lysate was probed in WB with anti-CD42/GPIb. Note the intact ~130-kDa GPIbα expression on platelets. (C) Platelet pellets or supernatants of WPs treated with Bar-III (4 µg) for 60 min at 37 °C. The positions of GPVI (~62-kDa) and the soluble GPVI fragment (~55-kDa) are indicated. C, platelet control. These results are representative of at least three similar experiments for each item.