Open AccessCXCL 12α/ SDF ‐1 from perisynaptic Schwann cells promotes regeneration of injured motor axon terminals
Author(s) -
Negro Samuele,
Lessi Francesca,
Duregotti Elisa,
Aretini Paolo,
La Ferla Marco,
Franceschi Sara,
Menicagli Michele,
Bergamin Elisanna,
Radice Egle,
Thelen Marcus,
Megighian Aram,
Pirazzini Marco,
Mazzanti Chiara M,
Rigoni Michela,
Montecucco Cesare
Publication year - 2017
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.201607257
Subject(s) - axon , regeneration (biology) , neuromuscular junction , microbiology and biotechnology , neuroscience , axon terminal , stromal cell , biology , motor neuron , spinal cord , cancer research
The neuromuscular junction has retained through evolution the capacity to regenerate after damage, but little is known on the inter‐cellular signals involved in its functional recovery from trauma, autoimmune attacks, or neurotoxins. We report here that CXCL 12α, also abbreviated as stromal‐derived factor‐1 ( SDF ‐1), is produced specifically by perisynaptic Schwann cells following motor axon terminal degeneration induced by α‐latrotoxin. CXCL 12α acts via binding to the neuronal CXCR 4 receptor. A CXCL 12α‐neutralizing antibody or a specific CXCR 4 inhibitor strongly delays recovery from motor neuron degeneration in vivo . Recombinant CXCL 12α in vivo accelerates neurotransmission rescue upon damage and very effectively stimulates the axon growth of spinal cord motor neurons in vitro . These findings indicate that the CXCL 12α‐ CXCR 4 axis plays an important role in the regeneration of the neuromuscular junction after motor axon injury. The present results have important implications in the effort to find therapeutics and protocols to improve recovery of function after different forms of motor axon terminal damage.