Figure 6.
Figure 6. The hypercoagulant state in Pon2−/−mice predominantly results from endothelial functions. (A) PT, (B) aPTT, and (C) tail-tip bleeding times Tek-Cre+/−Pon2ECrestored, Tek-Cre+/−, Pon2−/−, and WT mice (n = 12-29). Adjusted P values are indicated; Kruskal-Wallis test with Dunn multiple comparison. Scatter plots show results for individual mice, mean and SEM. (D-F) Similar analyses using BM chimeras and transplantation controls (n = 10-15), demonstrating a normalized coagulation time in WT chimera with Pon2−/−-derived BM. (G) PT and (H) aPTT of Pon2−/−-PAR2G37i, Pon2−/−, and WT mice (n = 10-23); Kruskal-Wallis test with Dunn multiple comparison.

The hypercoagulant state in Pon2−/−mice predominantly results from endothelial functions. (A) PT, (B) aPTT, and (C) tail-tip bleeding times Tek-Cre+/−Pon2ECrestored, Tek-Cre+/−, Pon2−/−, and WT mice (n = 12-29). Adjusted P values are indicated; Kruskal-Wallis test with Dunn multiple comparison. Scatter plots show results for individual mice, mean and SEM. (D-F) Similar analyses using BM chimeras and transplantation controls (n = 10-15), demonstrating a normalized coagulation time in WT chimera with Pon2−/−-derived BM. (G) PT and (H) aPTT of Pon2−/−-PAR2G37i, Pon2−/−, and WT mice (n = 10-23); Kruskal-Wallis test with Dunn multiple comparison.

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