Project description:Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived brain microvascular endotheial cells to identify alterations in gene expression. Methods: RNA were isolated from HD and control iPSC-derived brain microvascular endothelial cells. mRNAseq using Illumina TruSeq mRNA PolyA+ v2 lib prep and HiSeq 2500. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis. Results: mRNAseq and statistical analysis revealed differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells. Conclusions: Our study shows differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells, and reveals gene networks that are relevant to the mechanism of HD pathogenesis.
Project description:Huntington's disease (HD) is associated with dysfunction of the blood-brain barrier, including brain microvasscular endothelial cells (BMECs). We report changes in gene expression of induced pluripotent stem cells (iPSCs) and iPSC-derived brain microvascular endothelial cell-like cells (iBMECs) derived from an isogenic pair of iPSCs with either 180 (HD-corrected) or 18 (HD180) CAG repeats in the HTT gene.
Project description:Huntington's disease (HD) and control GLAST-postive induced pluripotent stem cell (iPSC)-derived astrocytes underwent single-nucleus RNA-sequencing to investigate cell state diversity across control and HD patient-derived astrocytes.
Project description:We report changes in gene expression from iPSC to iPSC-derived brain microvascular endothelial cells (dhBMECs) and from one-year cryopreservation of dhBMECs.
Project description:Huntington's disease is caused by an expanded CAG repeat in the huntingtin gene, yeilding a Huntingtin protein with an expanded polyglutamine tract. Patient-derived induced pluripotent stem cells (iPSCs) can help understand disease; however, defining pathological biomarkers in challanging. Here we used LC-MS/MS to determine differences in mitochondrial proteome between iPSC-derived neurons from healthy donors and Huntington's disease patients.
Project description:We aimed to investigate how transcription factors alter brain-specific and zonation-identity of endothelial cells. We used a dox-inducible lentivirus to increase expression of specific combinations of transcription factors expressed by human brain endothelial cells in iPSC-derived endothelial cell (iEC) monolayers. Using SMART-seq we compared gene expression profiles and benchmarked gene expression to iPSC-derived brain microvascular endothelial-like cells (iBMECs).
Project description:Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived neural cells to identify alterations in gene expression Methods: RNA were isolated from HD and control iPSC-derived neural cells. mRNAseq using Illumina Truseq mRNA PolyA+ v2 lib prep and Hiseq 2000. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis Results: mRNAseq and statistical analysis revealed 1869 differentially expressed genes between HD and control iPSC-derived neural cells. Conclusions: Our study shows 1869 differentially expressed genes between HD and control iPSC-derived neural cells, and reveals gene networks that relevant to the mechanism of HD pathogenesis.
Project description:To investigate the validity of using iPSC-derived brain microvascular endothelial-like cells (BMEC) as a model of human BMEC metabolism, we ran RNA-sequencing on iPSC-derived BMEC and compared gene expression of glycolytic and TCA enzymes to publically avaliable primary BMEC datasets.
