TY - JOUR
T1 - Autocrine hepatocyte growth factor provides a local mechanism for promoting axonal growth
AU - Yang, Xiu Ming
AU - Toma, Jean G.
AU - Bamji, Shernaz X.
AU - Belliveau, Daniel J.
AU - Kohn, Judi
AU - Park, Morag
AU - Miller, Freda D.
PY - 1998/10/15
Y1 - 1998/10/15
N2 - In this report, we describe a novel local mechanism necessary for optimal axonal growth that involves hepatocyte growth factor (HGF). Sympathetic neurons of the superior cervical ganglion coexpress bioactive HGF and its receptor, the Met tyrosine kinase, both in vivo and in vitro. Exogenous HGF selectively promotes the growth but not survival of cultured sympathetic neurons; the magnitude of this growth effect is similar to that observed with exogenous NGF. Conversely, HGF antibodies that inhibit endogenous HGF decrease sympathetic neuron growth but have no effect on survival. This autocrine HGF is required locally by sympathetic axons for optimal growth, as demonstrated using compartmented cultures. Thus, autocrine HGF provides a local, intrinsic mechanism for promoting neuronal growth without affecting survival, a role that may be essential during developmental axogenesis or after neuronal injury.
AB - In this report, we describe a novel local mechanism necessary for optimal axonal growth that involves hepatocyte growth factor (HGF). Sympathetic neurons of the superior cervical ganglion coexpress bioactive HGF and its receptor, the Met tyrosine kinase, both in vivo and in vitro. Exogenous HGF selectively promotes the growth but not survival of cultured sympathetic neurons; the magnitude of this growth effect is similar to that observed with exogenous NGF. Conversely, HGF antibodies that inhibit endogenous HGF decrease sympathetic neuron growth but have no effect on survival. This autocrine HGF is required locally by sympathetic axons for optimal growth, as demonstrated using compartmented cultures. Thus, autocrine HGF provides a local, intrinsic mechanism for promoting neuronal growth without affecting survival, a role that may be essential during developmental axogenesis or after neuronal injury.
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U2 - 10.1523/jneurosci.18-20-08369.1998
DO - 10.1523/jneurosci.18-20-08369.1998
M3 - Article
C2 - 9763480
AN - SCOPUS:0032531713
SN - 0270-6474
VL - 18
SP - 8369
EP - 8381
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 20
ER -