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- W4376104298 abstract "Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by motor neuron loss. Importantly, non-neuronal cell types such as astrocytes also play significant roles in disease pathogenesis. However, mechanisms of astrocyte contribution to ALS remain incompletely understood. Astrocyte involvement suggests that transcellular signaling may play a role in disease. We examined contribution of transmembrane signaling molecule ephrinB2 to ALS pathogenesis, in particular its role in driving motor neuron damage by spinal cord astrocytes. In symptomatic SOD1G93A mice (a widely-used ALS model), ephrinB2 expression was dramatically increased in ventral horn astrocytes. Reducing ephrinB2 selectively in these cervical spinal cord astrocytes via viral-mediated shRNA delivery reduced motor neuron loss and preserved respiratory function by maintaining phrenic motor neuron innervation of diaphragm. EphrinB2 expression was also elevated in human ALS spinal cord. These findings implicate ephrinB2 upregulation as both a transcellular signaling mechanism underlying astrocyte pathogenicity in ALS and a promising therapeutic target." @default.
- W4376104298 created "2023-05-12" @default.
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- W4376104298 date "2023-05-10" @default.
- W4376104298 modified "2023-09-26" @default.
- W4376104298 title "EphrinB2 knockdown in spinal cord astrocytes preserves diaphragm innervation in a mutant SOD1 mouse model of ALS" @default.
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- W4376104298 doi "https://doi.org/10.1101/2023.05.10.538887" @default.
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