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. Author manuscript; available in PMC: 2017 Sep 15.
Published in final edited form as: Blood Adv. 2017 Jun 23;1(15):1148–1158. doi: 10.1182/bloodadvances.2017005058

Figure 5. Genetic supplementation of APC by PC transgene expression.

Figure 5

(A–B) The D168F/N173K protein C transgene (mAPCHI) increased plasma levels of PC (A) and activated PC (B) as measured in mice with normal Thbd gene expression. To assess the expression of the mAPCHI transgene in the absence of endogenous aPC, PC-deficient mice with and without the transgene were added as additional experimental groups. Transgene-derived D168F/N173K PC expression was determined in APCHI mice lacking endogenous PC (PC−/−). Heterozygous PC-deficient mice (PC+/−) were included as controls. (C) The transgene partially restored the body weight of Thbd-null mice (for each time point: Thbd-null, n ≥ 24; mAPCHI Thbd-null, n ≥ 16; Thbd-expressing littermates, n ≥ 92). (D) D168F/N173K PC supplementation reduced mortality of tamoxifen-induced ERCre-ThbdloxP mice as well as of constitutively Thbd-deficient Meox2Cre-Thbd-null mice. (E) Pregnant Thbd-null mAPCHI mice showed pregnancy-induced bleeding, as shown by hemosiderin depositions in the lungs (left; original magnification 34, hematoxylin and eosin stain) and hemorrhage in the uterus (right).