Gene expression propionic patients, carriers, and controls
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE42816 | GEO | 2013/01/01
SECONDARY ACCESSION(S): PRJNA183488
REPOSITORIES: GEO
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Project description:In this study, we investigated PPA-induced changes in gene expression profiles of lymphoblastoid cell lines (LCLs) from unaffected individuals, compared with gene expression profiles of LCLs from sex-matched siblings with ASD. Global gene expression profiling analysis revealed that 96 genes in LCLs from the unaffected individuals were significantly altered after PPA exposure, exhibiting expression levels similar to those of their respective siblings with autism. Biological pathway analyses of these PPA-responsive genes suggested significant association with many neurological functions associated with autism, including synaptic transmission, neuronal cell differentiation and apoptosis. Moreover, we demonstrated that PPA also deregulated several of the responsive genes, including APOE, LIFR, NR3C1, and PTK2, in the neuroblastoma cell line SH-SY5Y. Functional analyses further showed that PPA exposure negatively impacted neurite outgrowth and promoted neurodegeneration in the human neuronal cell model. This study indicates that PPA exposure induces global changes in gene expression profiles of LCLs from non-autistic individuals that reflect expression patterns of LCLs from affected individuals.
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Project description:Baseline microRNA (miRNA) expression was evaluated in 107 HapMap lymphoblastoid cell lines (LCLs; 53 CEU and 54 YRI) using Exiqon miRCURY LNA arrays v10.0 (Exiqon array). Total RNA from each of the 107 HapMap sample was labeled and hybridized onto an Exiqon array
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Project description:In this study, we investigated PPA-induced changes in gene expression profiles of lymphoblastoid cell lines (LCLs) from unaffected individuals, compared with gene expression profiles of LCLs from sex-matched siblings with ASD. Global gene expression profiling analysis revealed that 96 genes in LCLs from the unaffected individuals were significantly altered after PPA exposure, exhibiting expression levels similar to those of their respective siblings with autism. Biological pathway analyses of these PPA-responsive genes suggested significant association with many neurological functions associated with autism, including synaptic transmission, neuronal cell differentiation and apoptosis. Moreover, we demonstrated that PPA also deregulated several of the responsive genes, including APOE, LIFR, NR3C1, and PTK2, in the neuroblastoma cell line SH-SY5Y. Functional analyses further showed that PPA exposure negatively impacted neurite outgrowth and promoted neurodegeneration in the human neuronal cell model. This study indicates that PPA exposure induces global changes in gene expression profiles of LCLs from non-autistic individuals that reflect expression patterns of LCLs from affected individuals. We conducted experiments using LCLs derived from individuals with ASD (n = 5) and their sex-matched unaffected siblings (n = 5). LCLs from non-ASD individuals were treated with 10 mM PPA, 10 mM propanol, or PBS. LCLs from individuals with ASD were treated with 10 mM propanol or PBS. At 24h after treatment, all LCLs were harvested. Gene expression profiling was conducted using TIGR 40K human cDNA microarrays. For each sample, total RNA was isolated and cDNA was synthesized, labeled with Cy-3 dye, and co-hybridized with Cy-5 labeled reference cDNA prepared from Universal human RNA (Stratagene, USA) on a TIGR 40K human cDNA microarray.
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