Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Keywords: gene expression study
Project description:Mutation in the huntingtin (HTT) gene causes Huntington’s disease. Wild type Htt is essential for development as Htt knockout mice die at day E7.5. Increasing evidence suggests mutant Htt may alter neurogenesis and development of striatal neurons resulting in neuronal loss. Using mouse embryonic stem cells (mESCs), we examined the role of Htt in neural differentiation. We found Htt-null (HN) mESCs inefficient in generating neural stem cells. In contrast differentiation into progenitors of mesoderm and endoderm lineages was not affected. To investigate the basis for the lack of neural differentiation, we carried out gene expression profiling by RNA-seq to examine if genes involved in neural differentiation were dysregulated in HN mESCs.
Project description:The aim of the study was to characterize the molecular mechanism involved in TGF-M-CM-^_ mediated smooth muscle formation in vitro. We employed rat bone marrow derived Oct4 expressing clones of multipotent adult progenitor cells (rMAPC). We subjected these cells to differentiation towards smooth muscle cell as previously reported using TGF-M-CM-^_1. The differentiation process reuires 6 days with media change every 2 days followed by RNA harvest. RNA was isolated using commercially available kits (Qiagen RNA easy micro kit). RNA integrity and quality was assessed prior to labeling and hybridization. As a control RNA from rat aortic smooth muscle cells was commercially obtained. Two biological replicate clones of rMAPC cells were used for the differentiation to smooth muscle like cells. The RNA was harvested at days 0, 2, 4 and 6 in triplicates. The RNA from primary smooth muscle cells was commercially obtained and was used in duplicates as control.
Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Experiment Overall Design: Primary neurons samples infected with TRE-Htt-N853-18Q or -82Q.
Project description:In this study, we conducted a comprehensive transcriptional profiling of the hippocampus utilizing a zQ175 knock-in (KI) mouse model of Huntington's disease, which was treated with either HTT-10150 siRNA specifically designed to target the full-length huntingtin (Htt) mRNA or combination of HTT-634 and HTT-486 siRNAs targeting HTT1a. Our investigation aimed to assess the impact of this intervention across different time points.