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The Journal of Neuroscience, August 1, 2002, 22(15):6537-6548

Overexpression of HGF Retards Disease Progression and Prolongs Life Span in a Transgenic Mouse Model of ALS

Woong Sun*, Hiroshi Funakoshi*, and Toshikazu Nakamura

Division of Molecular Regenerative Medicine, Course of Advanced Medicine, Osaka University Graduate School of Medicine, B-7, Osaka 565-0871, Japan

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a progressive loss of motoneurons and degeneration of motor axons. We show that overexpression of hepatocyte growth factor (HGF) in the nervous system attenuates motoneuron death and axonal degeneration and prolongs the life span of transgenic mice overexpressing mutated Cu2+/Zn2+ superoxide dismutase 1. HGF prevented induction of caspase-1 and inducible nitric oxide synthase (iNOS) in motoneurons and retained the levels of the glial-specific glutamate transporter (excitatory amino acid transporter 2/glutamate transporter 1) in reactive astrocytes. We propose that HGF may be the first example of an endogenous growth factor that can alleviate the symptoms of ALS by direct neurotrophic activities on motoneurons and indirect activities on glial cells, presumably favoring a reduction in glutamatergic neurotoxicity.

Key words: HGF; c-Met; amyotrophic lateral sclerosis; caspase-1; EAAT2; motoneuron

* W.S. and H.F. contributed equally to this work.

Copyright © 2002 Society for Neuroscience  0270-6474/02/22156537-12$05.00/0


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