期刊
EMBO MOLECULAR MEDICINE
卷 9, 期 8, 页码 1000-1010出版社
WILEY
DOI: 10.15252/emmm.201607257
关键词
CXCL12; CXCR4; neuromuscular junction; neuroregeneration; perisynaptic Schwann cells
资金
- Fondazione CARIPARO
- Provincia autonoma di Trento (Bando Grandi Progetti, AXonomIX)
- Interomics project of the CNR
- Fondazione Pisana per la Scienza
- Italian Ministry of Health [GR-2010-2320779]
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 CXCL12, also abbreviated as stromal-derived factor-1 (SDF-1), is produced specifically by perisynaptic Schwann cells following motor axon terminal degeneration induced by -latrotoxin. CXCL12 acts via binding to the neuronal CXCR4 receptor. A CXCL12-neutralizing antibody or a specific CXCR4 inhibitor strongly delays recovery from motor neuron degeneration invivo. Recombinant CXCL12 invivo accelerates neurotransmission rescue upon damage and very effectively stimulates the axon growth of spinal cord motor neurons invitro. These findings indicate that the CXCL12-CXCR4 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.
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