Researchers at Hong Kong University of Science and Technology (HKUST) report success in prompting severed axons in mice to regenerate, raising hopes for the development of viable treatments for spinal cord injuries.
Central nervous system damage (CNS) damage can result in permanent loss of sensory and motor function because severed axons are unable to regenerate. There are currently very limited options to help these patients regain their motor abilities, and researchers have been exploring ways to enable the regeneration of severed axons.
Peripheral nerves have stronger ability than the CNS to regrow and repair following injury, but scientists have yet to fully understand the relationship between this self-repair and the intrinsic immune mechanism of the nervous system. The HKUST team wanted to whether immune-related signaling pathways affected neurons after injury, and whether they could enhance axonal regeneration directly.
Led by Cheng Associate Professor Kai Liu of the Division of Life Science, the HKUST team found that the deletion of PTPN2, a phosphatase-coding gene, in neurons can prompt axons to regrow. When combined with the type II interferon IFNγ, it can further accelerate the process and boost the number of axons regenerated. The results have recently been published in the scientific journal Neuron.
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The study investigated whether the signaling pathway IFNγ-cGAS-STING had any role in the regeneration process of peripheral nerves. Researchers found that peripheral axons could directly modulate the immune response in their injured environment to promote self-repair after injury.
In previous research, Liu’s team demonstrated that elevating the neuronal activity and regulating the neuronal glycerolipid metabolism pathway could boost axon regenerative capacity. The current study provides further insights into the search of treatment solutions for challenging conditions such as spinal cord injuries, with one possible option being the joining of several types of different signaling pathways.