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Exploitable, highly context-specific astrocytes

ABSTRACT: To investigate the functional heterogeneity of astrocytes from a defined brain region, we designed 14 experimental manipulations including Huntington's disease models, pathological challenges, ionic and GPCR signaling alterations, and analyzed the transcriptomic profiles of striatal astrocytes. From the analyses, we have identified context-specific changes of striatal astrocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE153791 | GEO | 2020/11/17

REPOSITORIES: GEO

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Exploitable, highly context-specific astrocytes

Project description:To investigate the functional heterogeneity of astrocytes from a defined brain region, we designed 12 experimental manipulations including Huntington's disease models, pathological challenges, ionic and GPCR signaling alterations, and analyzed the transcriptomic profiles of striatal astrocytes. From the analyses, we have identified context-specific changes of striatal astrocytes.

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Project description:Glial pathology has been implicated as a causal contributor to the dysfunction and death of striatal neurons that characterizes Huntington disease. In this study, we investigated mutant HTT (mHTT)-associated changes in gene expression by both mouse and human striatal astrocytes. Mouse striatal astrocytes were FACS-sorted from two distinct models, R6/2 and zQ175 mice, which respectively express exon1-only truncated or full-length HTT, while human astrocytes were generated from either hESCs expressing full-length mHTT, or fetal striatal glia transduced with exon1-only mHTT. Comparison of differential gene expression between each of these conditions and their normal HTT controls, and to one another, revealed astrocyte-specific alterations in both truncated and full-length mHTT models that were shared by both species, yet with differences that clearly distinguished glia derived from each model. Overlap of these data sets revealed that the patterns of mHTT-associated transcriptional dysregulation depended not only upon species, but also upon whether the astroglia expressed truncated or full-length mHTT. These data revealed a common set of conserved, mHTT-associated dysregulated pathways that may present targets for the rescue of glial pathology in HD, while revealing that the gene expression of glia expressing truncated mHTT may differ substantially from that of glia expressing full-length mHTT.

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