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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: J Thromb Haemost. 2018 May 8;16(6):1211–1225. doi: 10.1111/jth.14005

Figure 6. Pharmacologic inhibition or genetic ablation of PDK1 delays pulmonary thromboembolism induced mortality.

Figure 6

(A) Wildtype mice were treated with BX-795 (10 μg/ml) or vehicle (DMSO) by intraperitionial injection once a day for 0, 3, or 5 days. Phosphorylation of Akt (T308) in isolated platelets stimulated with 2MeSADP ex vivo was measured to determine the duration of BX-795 treatment necessary to completely block phosphorylation of AKT. (B) Wildtype mice were treated with different concentrations of BX-795 (or vehicle) by intraperitoneal injection once a day for 5 days at various concentrations. Phosphorylation of Akt (T308) in isolated platelets stimulated with 2MeSADP ex vivo was measured. For Panels A and B, actin is a loading control and the immunoblot is representative of n=3 independent experiments. (C, D) Wildtype mice were treated with BX795 (10 μg/ml) or vehicle for 5 days. Pulmonary thromboembolism was induced by injecting (C) 2MeSADP (20mg/kg) plus epinephrine (30mg/kg) or (D) collagen (0.4 mg/kg) plus epinephrine (30mg/kg). N=7 mice/group for Panels C and D. Representative histological sections from lungs of mice injected with ADP are shown above. (E) pdk1fl/fl or pdk1−/− mice after induction of pulmonary thromboembolism (n=6/group). Representative histological sections from pdk1fl/fl or pdk1−/−lungs are shown to the right.