Figure 7
Figure 7. NGF-β–enhanced migratory properties of CD117+ cells from the blood. (A) Relative change of the migratory activity of human peripheral CD117+ progenitor cells from healthy control participants (CTR; n = 12 for NGF; n = 6 for BDNF, NT-3, and NT-4) and patients with mastocytosis (MAST; n = 6; n = 1 for CM, n = 4 for ISM, and n = 1 for SSM) toward a NGF-β, BDNF, NT-3, and NT-4 gradient in transwell chamber experiments compared with unstimulated control participants is shown as mean values and SEMs. (B) Number of human peripheral migrated CD117+ progenitor cells from healthy control participants (n = 4) toward a NGF-β gradient increases in a dose-dependent fashion. (C) Addition of anti-human TrkA antibody significantly prevented migration of CD117+ cells toward NGF-β in both patients with mastocytosis and healthy control participants (n = 6 each), indicating that NGF-β–driven migration of CD117+ cells was mainly mediated via TrkA.

NGF-β–enhanced migratory properties of CD117+cells from the blood. (A) Relative change of the migratory activity of human peripheral CD117+ progenitor cells from healthy control participants (CTR; n = 12 for NGF; n = 6 for BDNF, NT-3, and NT-4) and patients with mastocytosis (MAST; n = 6; n = 1 for CM, n = 4 for ISM, and n = 1 for SSM) toward a NGF-β, BDNF, NT-3, and NT-4 gradient in transwell chamber experiments compared with unstimulated control participants is shown as mean values and SEMs. (B) Number of human peripheral migrated CD117+ progenitor cells from healthy control participants (n = 4) toward a NGF-β gradient increases in a dose-dependent fashion. (C) Addition of anti-human TrkA antibody significantly prevented migration of CD117+ cells toward NGF-β in both patients with mastocytosis and healthy control participants (n = 6 each), indicating that NGF-β–driven migration of CD117+ cells was mainly mediated via TrkA.

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