Lysosomal and network alterations in human mucopolysaccharidosis type VII iPSC-derived neurons View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Neus Bayó-Puxan, Ana Paula Terrasso, Sophie Creyssels, Daniel Simão, Christina Begon-Pescia, Marina Lavigne, Sara Salinas, Florence Bernex, Assumpció Bosch, Vasiliki Kalatzis, Thierry Levade, Ana Maria Cuervo, Philippe Lory, Antonella Consiglio, Catarina Brito, Eric J. Kremer

ABSTRACT

Mucopolysaccharidosis type VII (MPS VII) is a lysosomal storage disease caused by deficient β-glucuronidase (β-gluc) activity. Significantly reduced β-gluc activity leads to accumulation of glycosaminoglycans (GAGs) in many tissues, including the brain. Numerous combinations of mutations in GUSB (the gene that codes for β-gluc) cause a range of neurological features that make disease prognosis and treatment challenging. Currently, there is little understanding of the molecular basis for MPS VII brain anomalies. To identify a neuronal phenotype that could be used to complement genetic analyses, we generated two iPSC clones derived from skin fibroblasts of an MPS VII patient. We found that MPS VII neurons exhibited reduced β-gluc activity and showed previously established disease-associated phenotypes, including GAGs accumulation, expanded endocytic compartments, accumulation of lipofuscin granules, more autophagosomes, and altered lysosome function. Addition of recombinant β-gluc to MPS VII neurons, which mimics enzyme replacement therapy, restored disease-associated phenotypes to levels similar to the healthy control. MPS VII neural cells cultured as 3D neurospheroids showed upregulated GFAP gene expression, which was associated with astrocyte reactivity, and downregulation of GABAergic neuron markers. Spontaneous calcium imaging analysis of MPS VII neurospheroids showed reduced neuronal activity and altered network connectivity in patient-derived neurospheroids compared to a healthy control. These results demonstrate the interplay between reduced β-gluc activity, GAG accumulation and alterations in neuronal activity, and provide a human experimental model for elucidating the bases of MPS VII-associated cognitive defects. More... »

PAGES

16644

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41598-018-34523-3

    DOI

    http://dx.doi.org/10.1038/s41598-018-34523-3

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1108043139

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30413728


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