Project description:We used the microarray to investigate the lack of Tenascin-R in brain of adult and P7 mice. The aim was to find differential expressed genes which could explain the behaviour differences between the tenascin wt and ko mice. The data show that not many genes are dysregulated in the Tnr deficient mouse in comparison to the wt mouse brain. Gas5 was one of the dysregulated genes. Gas5 was dysregulated in the P7 and 2 month old mice. Experiment Overall Design: 14: (P7 4wt vs 4ko), (adult 3wt vs 3ko)
Project description:We used the microarray to investigate the lack of Tenascin-R in brain of adult and P7 mice. The aim was to find differential expressed genes which could explain the behaviour differences between the tenascin wt and ko mice. The data show that not many genes are dysregulated in the Tnr deficient mouse in comparison to the wt mouse brain. Gas5 was one of the dysregulated genes. Gas5 was dysregulated in the P7 and 2 month old mice.
Project description:Transcriptional profiling of mouse esophageal development. Goal was to globally profile critical genes and signaling pathways during the development of mouse esophagus and determine how Nrf2/Keap1 pathway regulates the morphogenesis of the esophageal epithelium. Mutiple-comparison. WT-E11.5 vs. WT-E15.5 vs. WT-P0 vs. WT-P7; WT-P7 vs. WT-adult; WT-adult vs. Nrf2-/--adult; WT-P7 vs. Nrf2-/--P7 vs. Keap1-/--P7 vs. Nrf2-/-Keap1-/--P7. Biological replicates: 3 replicates for each group.
Project description:In order to investigate what signalling pathways are turned on by tenascin-C, we generated Mouse Embryonic Fibroblasts (MEFs) deficient for tenascin-C and compared their gene expression profile to MEFs proficient for tenascin-C. TNC-KO MEFs as well as WT MEFs in which tenascin-C was knocked-down (following stable transfection of a short hairpin RNA) were compared to WT MEFs (expressing strong endogenous levels of tenascin-C).
Project description:This SuperSeries is composed of the following subset Series: GSE8549: Transcriptome of reloaded soleus muscle of 129/SV mice GSE8550: Transcriptome of soleus muscle of Tenascin-C deficient 129/SV mice GSE8551: Transcriptome of reloaded soleus muscle of Tenascin-C deficient 129/SV mice GSE8552: Transcriptome of soleus muscle of 129/SV mice Keywords: SuperSeries Refer to individual Series
Project description:The extracellular matrix (ECM) molecules tenascin-C (Tnc), tenascin-R (Tnr), brevican (Bcan) and neurocan (Ncan) are completely knocked out in the quadruple knockout mouse. This removal of these central ECM molecules lead to an altered gene expression in the hippocampus of postnatal day (P) 21 old quadruple knockout mice. Among others, the expression of genes involved in the process of synapse formation associated with synaptic transmission were significantly changed in the quadruple knockout hippocampus compared to the wildtype hippocampus. We found e.g. an upregulated expression of Gamma-aminobutyric acid receptor subunit theta (Gabrq), Glutamate decarboxylase (Gad2) and semaphorin 4c (Sema4c), which are known contributors at synapses. Interestingly, some extracellular molecules e.g. like glypican 3 (Gpc3), calreticulin (Calr) and three different types of collagens (Col1a2, Col4a3 and Col27a1) showed also a modified expression. These data indicate the importance of the four ECM molecules for an intact gene expression in the murine hippocampus.
Project description:Adult neurogenesis, found in two neurogenic regions of the brain, has profound roles in neural plasticity and brain function. A hallmark feature of neurodegeneration is neuroinflammation, which can either enhance or inhibit neurogenesis depending on the context of the brain microenvironment. The consequences of deficient DNA repair in adult neurogenesis and neuroinflammation are poorly understood despite their potential relevance for homeostasis. We previously reported that loss of NEIL1, an important DNA glycosylase involved in DNA base excision repair, is associated with deficiencies in spatial memory, olfaction, and protection against ischemic stroke in mice. Here, we show that Neil1-/- mice display an anxiety-mediated behavior in the open field test, a deficient recognitive memory in novel object recognition and increased neuroinflammatory response under basal conditions. Further, mice lacking NEIL1 have decreased neurogenesis and deficient resolution of neuroinflammation following gamma irradiation (IR)-induced stress compared to WT mice. Neil1-/- IR-exposed mice also exhibit increased DNA damage and apoptosis in the hippocampus. Interestingly, behavioral tests two weeks after IR showed impaired stress response in the Neil1-/- mice. Our data indicate that NEIL1 plays an important role in adult neurogenesis and in the resolution of neuroinflammation.
