Figure 1
Figure 1. VEGFR1 stimulation, but not VEGFR2 stimulation, is responsible VEGF-A165–induced thrombocytosis. (A-B) Mice were administered either VEGF-A165 (100 μg/kg intraperitoneally), PlGF-2, VEGF-E (100 μg/kg intraperitoneally), or vehicle (PBS) each day for 4 consecutive days. (A) Some groups of mice receiving the 4-day VEGF-A165 regimen were also administered blocking Abs to either VEGFR1, VEGFR2, VEGFR1&2, or control IgG 20 minutes before VEGF-A165 administration on days 1 and 3. Enumeration of circulating platelets was then conducted 24 hours after last growth factor administration. Bone marrow or spleens were also harvested, and MKs were identified by flow cytometry via forward and side scatter and CD41 expression. (C) Percentage of MKs expressing VEGFR1 and VEGFR2 in vehicle control–treated mice. (D) The number of MKs per million cells from bone marrow or spleen; n = 5-6 animals per group. Data are expressed as mean ± SEM; *P < .05; ***P < .001 compared with control or as indicated.

VEGFR1 stimulation, but not VEGFR2 stimulation, is responsible VEGF-A165–induced thrombocytosis. (A-B) Mice were administered either VEGF-A165 (100 μg/kg intraperitoneally), PlGF-2, VEGF-E (100 μg/kg intraperitoneally), or vehicle (PBS) each day for 4 consecutive days. (A) Some groups of mice receiving the 4-day VEGF-A165 regimen were also administered blocking Abs to either VEGFR1, VEGFR2, VEGFR1&2, or control IgG 20 minutes before VEGF-A165 administration on days 1 and 3. Enumeration of circulating platelets was then conducted 24 hours after last growth factor administration. Bone marrow or spleens were also harvested, and MKs were identified by flow cytometry via forward and side scatter and CD41 expression. (C) Percentage of MKs expressing VEGFR1 and VEGFR2 in vehicle control–treated mice. (D) The number of MKs per million cells from bone marrow or spleen; n = 5-6 animals per group. Data are expressed as mean ± SEM; *P < .05; ***P < .001 compared with control or as indicated.

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