Figure 4.
Figure 4. Protease signaling in endothelial cells from Par1–/–:Par2–/– mice. Dermal microvascular endothelial cells isolated from Par1–/–:Par2–/– neonates or matched controls were serum-starved, loaded with 3H-inositol, and exposed to vehicle, protease, or agonist peptide as indicated. To exclude nonspecific responses to contaminating thrombin, hirudin was included with all proteases except thrombin. Results from 2 independent experiments are shown. Each bar represents 1 experiment done in triplicate; error bars show standard deviation. Par1–/–:Par2–/– cells did respond to nonprotease agonists such as serum and lysophosphatidic acid; h indicates human; m, mouse.

Protease signaling in endothelial cells from Par1/:Par2/ mice. Dermal microvascular endothelial cells isolated from Par1/:Par2/ neonates or matched controls were serum-starved, loaded with 3H-inositol, and exposed to vehicle, protease, or agonist peptide as indicated. To exclude nonspecific responses to contaminating thrombin, hirudin was included with all proteases except thrombin. Results from 2 independent experiments are shown. Each bar represents 1 experiment done in triplicate; error bars show standard deviation. Par1/:Par2/ cells did respond to nonprotease agonists such as serum and lysophosphatidic acid; h indicates human; m, mouse.

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