Linoleic acid improves PIEZO2 dysfunction in a mouse model of Angelman Syndrome.
Luis O RomeroRebeca CairesA Kaitlyn VictorJuanma RamirezFrancisco J Sierra-ValdezPatrick WalshVincent TruongJungsoo LeeUgo MayorLawrence T ReiterValeria VásquezJulio F Cordero-MoralesPublished in: Nature communications (2023)
Angelman syndrome (AS) is a neurogenetic disorder characterized by intellectual disability and atypical behaviors. AS results from loss of expression of the E3 ubiquitin-protein ligase UBE3A from the maternal allele in neurons. Individuals with AS display impaired coordination, poor balance, and gait ataxia. PIEZO2 is a mechanosensitive ion channel essential for coordination and balance. Here, we report that PIEZO2 activity is reduced in Ube3a deficient male and female mouse sensory neurons, a human Merkel cell carcinoma cell line and female human iPSC-derived sensory neurons with UBE3A knock-down, and de-identified stem cell-derived neurons from individuals with AS. We find that loss of UBE3A decreases actin filaments and reduces PIEZO2 expression and function. A linoleic acid (LA)-enriched diet increases PIEZO2 activity, mechano-excitability, and improves gait in male AS mice. Finally, LA supplementation increases PIEZO2 function in stem cell-derived neurons from individuals with AS. We propose a mechanism whereby loss of UBE3A expression reduces PIEZO2 function and identified a fatty acid that enhances channel activity and ameliorates AS-associated mechano-sensory deficits.
Keyphrases
- poor prognosis
- spinal cord
- intellectual disability
- mouse model
- endothelial cells
- induced pluripotent stem cells
- binding protein
- autism spectrum disorder
- fatty acid
- physical activity
- long non coding rna
- adipose tissue
- small molecule
- type diabetes
- spinal cord injury
- body mass index
- metabolic syndrome
- cerebral palsy
- skeletal muscle
- cell migration
- protein protein
- amino acid