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Blood, Vol. 95 No. 6 (March 15), 2000:
pp. 2052-2058
Nerve growth factor functions as a chemoattractant for mast
cells through both mitogen-activated protein kinase and
phosphatidylinositol 3-kinase signaling pathways
Junko Sawada,
Atsuko Itakura,
Akane Tanaka,
Tohru Furusaka, and
Hiroshi Matsuda
From the Department of Veterinary Clinic, Faculty of Agriculture,
Tokyo University of Agriculture and Technology, Fuchu; and the
Department of Otolaryngology, Nihon University School of Medicine,
Chiyoda-ku, Tokyo, Japan.
Despite being a well-characterized neurotrophic factor, nerve growth
factor (NGF) influences survival, differentiation, and functions of
mast cells. We investigated whether NGF was able to induce directional
migration of rat peritoneal mast cells (PMCs). NGF clearly induced
chemotactic movement of PMCs in a dose-dependent manner with the
drastic morphological change and distribution of F-actin, which was
completely blocked by pretreatment with Clostridium botulinum
C2 toxin, an actin-polymerization inhibitor. Because PMCs constitutively express the NGF high-affinity receptor (TrkA) with a tyrosine kinase domain, we focused on downstream effectors in signaling cascades following the TrkA. NGF rapidly activated both mitogen-activated protein kinase (MAPK) and
phosphatidylinositol 3-kinase (PI3K), and the addition of inhibitors
specific for MAPK kinase and PI3K suppressed cell migration and these
signals. In the coculture system with PMCs and fibroblasts, which
produce biologically active NGF, directional migration of PMCs to
fibroblasts was observed, and the addition of anti-NGF polyclonal
antibodies significantly suppressed the migration of PMCs. These
findings suggested that NGF initiated chemotactic movement of PMCs
through both MAPK and PI3K signaling pathways following TrkA
activation. Thus, locally produced NGF may play an important role in
mast cell accumulation in allergic and nonallergic inflammatory conditions.
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