The molecular mechanisms underlying the changes in the nigrostriatal pathway in Parkinsons disease (PD) are not completely understood. Here we use microarrays and mass spectrometry to study the transcriptomic and proteomic changes in the striatum of two mouse models of PD induced by distinct neurotoxins, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and methamphetamine (METH). Transcripts and proteins were found with similar abundance changes in both models which may be involved in the pathophysiology of PD. GFAP transcript and protein levels were significantly up-regulated by both neurotoxins, confirming the known astrocytic response to these drugs. Other genes and proteins were idiosyncratic in their responses to the two toxins, suggesting specific toxicological responses. Comparing transcript and protein levels revealed that efficiently translated genes used more commonly occurring codons than inefficiently translated genes. Additionally, a potential role was found for miRNAs in translational control in the striatum. The results constitute one of the largest datasets integrating transcript and protein changes for these two neurotoxin models with many similar endpoint phenotypes but distinct pathologies. Using multiple toxins while examining proteins and transcripts can be an effective method of delineating the molecular pathology of neurodegenerative diseases.
Mitochondrial dysfunction, oxidative stress, and apoptosis revealed by proteomic and transcriptomic analyses of the striata in two mouse models of Parkinson's disease.
Sex, Age, Specimen part
View SamplesThe purpose of this study was to characterize the gene expression profile of MDA-MB-231 breast cancer cells treated with various SCFA-hexosamine analogs to better understand the role of various modifications to this scaffold.
Hexosamine template. A platform for modulating gene expression and for sugar-based drug discovery.
No sample metadata fields
View SamplesCorticospinal motor neurons (CSMN) are one specialized class of cortical excitatory neurons, which connect layer Vb of the cortex to the spinal cord. a master transcription factor Forebrain expressed zinc finger 2 (Fezf2) has been identified that is necessary for the fate specification of CSMN. Fezf2 alone can cell-autonomously instruct the acquisition of CSMN-specific features when expressed in diverse, permissive cellular contexts, in vivo.
Gene co-regulation by Fezf2 selects neurotransmitter identity and connectivity of corticospinal neurons.
No sample metadata fields
View SamplesIn this study, we have explored microarray-based differential gene expression profile in mouse lung tissue 8 h after inducing polymicrobial sepsis and the effect of preprotachykinin-A (PPTA) gene deletion. A range of genes differentially expressed (> 2-fold) in microarray analysis was assessed, PPTA-knockout septic mice with their respective sham controls.
Substance P in polymicrobial sepsis: molecular fingerprint of lung injury in preprotachykinin-A-/- mice.
Specimen part, Treatment
View SamplesInhibition of proteasome degradation pathway has been implicated in neuronal cell death leading to neurodegenerative diseases such as Parkinsons disease and Alzheimers disease. Pharmacological proteasomal inhibitors such as lactacystin can induce apoptosis in cultured mouse cortical neurons through the activation of caspase-3. Furthermore, proteasomal inhibitors are also reported to mediate deleterious alterations in cell cycle regulation, inflammatory processes and protein aggregation and trigger the cell death pathway.
Up-regulation of endoplasmic reticulum stress-related genes during the early phase of treatment of cultured cortical neurons by the proteasomal inhibitor lactacystin.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A global transcriptomic view of the multifaceted role of glutathione peroxidase-1 in cerebral ischemic-reperfusion injury.
Treatment
View SamplesIschemic stroke triggers severe focal hypoperfusion accompanied with deprivation of oxygen and glucose to the cerebral tissue, together with loss of ATP, depolorization of neurons, elevated extracellular potassium concentration, and subsequently leads to excitotoxicity as well as increased oxidative stress promoting microvascular injury, blood-brain-barrier deregulation, post-ischemic inflammation and eventually the consequential neurological deficit. Although reperfusion of ischemic brain tissue is critical for restoring normal function, it can paradoxically result in secondary damage, called ischemia/reperfusion (I/R) injury.
A global transcriptomic view of the multifaceted role of glutathione peroxidase-1 in cerebral ischemic-reperfusion injury.
Treatment
View SamplesTo investigate the molecular bases of diet induced differences in milk composition, we collected milk from mid lactation dairy ewes and after 3 weeks of diet supplementation with extruded linseed. RNAs were isolated from milk somatic cells isolated from milk of 3 sheep and Illumina RNA sequencing was performed to analyze RNA synthesis in these cells. Overall design: Transcriptional profiling of milk somatic cells of sheep fed with normal diet and with a supplementation with extruded linseed. Sequence data were generated by deep sequencing, on three replicates, using Illumina HiSeq2000.
Transcript profiling in the milk of dairy ewes fed extruded linseed.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide methylation analysis in vestibular schwannomas shows putative mechanisms of gene expression modulation and global hypomethylation at the HOX gene cluster.
Specimen part
View SamplesBackground: Schwannomas and grade I meningiomas are non-metastatic neoplasms that shares the common mutation of gene NF2. They usually appear in Neurofibromatosis type 2 patients. Currently, there is no drug treatment available for both tumors, so the use of wide expression technologies is crucial to find those therapeutic targets.
Global expression profile in low grade meningiomas and schwannomas shows upregulation of PDGFD, CDH1 and SLIT2 compared to their healthy tissue.
Specimen part
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