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 2
PC levels correlate with poor survival in unchallenged low-PC mice. (A) Plasma PC levels were measured in mice derived from WT and the various low-PC transgenic lines using ELISA methodology. In PC^–/–(PC^Tg535), PC^–/–(PC^Tg4), PC^–/–(PC^Tg785), and PC^–/–(PC^Tg527) mice, the levels of plasma PC represents less than 1%, 1%, 3%, and 18% of age- and gender-matched WT plasma respectively. (B) Survival of mixed-gender progenies derived from various PC transgenic lines. The values in parentheses indicate the PC levels in the corresponding strains as percent of WT values. PC^–/–(PC^Tg535) offspring (n = 46) had the poorest survival and the lowest PC levels compared with progenies from PC^–/–(PC^Tg527) (n = 49), PC^–/–(PC^Tg785) (n = 144), or PC^–/–(PC^Tg4) (n = 63) strains. The disease onset and death in PC^–/–(PC^Tg535) littermates occurred at a young age (<1 month). In contrast, offspring from PC^–/–(PC^Tg4) and PC^–/–(PC^Tg785) mice had late-onset thrombotic phenotypes and accordingly longer survival. Progenies from PC^–/–(PC^Tg527) mice lacked spontaneous phenotypes and developed normally.