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 3
Gross phenotypes of the low-PC transgenic mice. (A and B) Early onset of severe hemorrhage in the tails and legs of PC^–/–(PC^Tg535) littermates. (C–G) Late onset of thromboembolic phenotypes in PC^–/–(PC^Tg785) and PC^–/–(PC^Tg4) offspring characterized by hemorrhagic skin lesions affecting various parts of the body (C: tail; D and E: paws; F: ear; G: face). (H and I) Specimens collected from PC^–/–(PC^Tg785) mice euthanized due to illness. Multiple focal hemorrhagic lesions in the lung (H) and muscle (I) of the legs. (J) Severe necrosis of regions of the liver. (K) Tail bleeding times were measured in PC^–/–(PC^Tg785) mice of various ages. The data are expressed as the fraction still bleeding as a function of time. No statistical differences were found in bleeding times between 8- and 12-week-old WT mice. In contrast, low-PC mice at 8 weeks showed significantly shorter bleeding times compared with WT mice, while the 12-week-old low-PC mice had significantly prolonged bleeding times compared with 8-week-old low-PC or WT mice.