Mice with a severe deficiency in protein C display prothrombotic and proinflammatory phenotypes and compromised maternal reproductive capabilities
J. Clin. Invest. Angelina J. Lay, et al. 115:1552
doi:10.1172/JCI24030 [Go to this article.]

Figure 6
Spontaneous abortion in PC–/–(PCTg785) mothers. (A and B) H&E stains of embryos in utero showing enhanced bleeding and fibrin deposition at the ectoplacental cone region and area surrounding a 6.5-dpc embryo. (C and D) Intense fibrin depositions were present in 7.5-dpc embryos in PC–/–(PCTg785) mothers. However, proliferation of trophoblast giant cells remained comparable to that in WT mice (data not shown). (E and F) Immunohistochemical staining using the TUNEL assay revealed extensive trophoblast giant cell death in PC–/–(PCTg785) mothers. H&E staining of WT (G) and low-PC (H) 8.5-dpc embryos highlighting severe growth retardation and partially resorbed embryos accompanied by severe uterine bleeding in PC–/–(PCTg785) mothers. (I and J) Enhanced inflammation at the ectoplacental cone region as illustrated by increased anti-CD45 positive leukocyte infiltration in PC–/–(PCTg785) compared with WT mothers. Asterisks indicate ectoplacental cone region.