Serum microRNA expression prior to motion sickness stimulus
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ABSTRACT:
PROVIDER: PRJNA852603 | ENA |
REPOSITORIES: ENA
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2015-01-08 | E-MTAB-3213 | biostudies-arrayexpress
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2024-07-26 | PXD054312 |
Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of two isogenic T.b.gambiense lines that are either sensitive or resistant to human serum.
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2018-06-18 | E-MTAB-5614 | biostudies-arrayexpress
Project description:Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy. Transgenic Mice and Neonatal Mouse Myocyte Culture: WT no serum, 5; WT with serum, 7; TG no serum, 6; TG with serum, 7.
2010-04-08 | E-GEOD-14288 | biostudies-arrayexpress
Project description:During neurogenesis, expression of the basic Helix-Loop-Helix NeuroD6/Nex1/MATH-2 transcription factor parallels neuronal differentiation, while maintaining the differentiated state in the mature nervous system. To further dissect NeuroD6 differentiation properties, we previously generated a NeuroD6-overexpressing stable PC12 cell line, PC12-ND6, which displays a neuronal phenotype characterized by spontaneous neuritogenesis, accelerated NGF-induced differentiation, and increased regenerative capacity. Furthermore, we reported that NeuroD6 promotes long-term neuronal survival upon oxidative stress triggered by serum deprivation. In this study, we identified the NeuroD6-mediated transcriptional regulatory pathways linking neuronal differentiation to survival, by conducting a genome-wide microarray analysis using PC12-ND6 cells and serum deprivation as a stress paradigm. Through a series of filtering steps and a gene-ontology analysis, we found that NeuroD6 promotes distinct but overlapping gene networks, consistent with the differentiation, regeneration, and survival properties of PC12-ND6 cells. Using a gene set enrichment analysis, we provide the first evidence of a compelling link between NeuroD6 and a set of heat shock proteins in the absence of stress, which may be instrumental to confer stress tolerance to PC12-ND6 cells. Immunocytochemistry results showed that HSP27 and HSP70 interact with cytoskeletal elements, consistent with their roles in neuritogenesis and preserving cellular integrity. HSP70 also colocalizes with mitochondria located in the soma, growing neurites and growth cones of PC12-ND6 cells prior to and upon stress stimulus, consistent with its neuroprotective functions. Collectively, our findings support the notion that NeuroD6 links neuronal differentiation to survival via the network of molecular chaperones and endows the cells with increased stress tolerance. Experiment Overall Design: The experimental design involved six replicates of serum-grown PC12 cells (control), serum-grown PC12-ND6 cells (t=0), and serum-deprived PC12-ND6 cells (t=48 hrs).
2009-05-11 | E-GEOD-15942 | biostudies-arrayexpress
Project description:Explore the effect of grass sickness on the equine faecal microbiome.
| PRJEB11642 | ENA
Project description:Background: The effects of iron deficiency anemia (IDA) during infancy extend beyond the hematologic compartment and include short- and long-term adverse effects on many tissues including the brain. However, biomarkers of iron-dependent brain health are lacking in humans. Prior analyses in rhesus infants indicated abnormal serum and cerebral spinal fluid (CSF) multiomic profiles both prior to and during IDA, characterized by alterations suggestive of hepatic and brain metabolic dysfunction, and impaired energy metabolism. Objective: To determine whether serum and CSF biomarkers of iron deficiency (ID)-induced metabolic dysfunction are concordant in the pre/early anemic stage of ID in a nonhuman primate model of infantile IDA. Methods: Paired serum and CSF specimens were collected from iron-sufficient (IS; n = 12) and ID (n = 7) rhesus infants at 4-months (preanemic period) and 6-months (anemic period) of age. Hematological, metabolomic, and proteomic profiles were generated via HPLC/MS at both timepoints to discover serum biomarkers of ID-induced brain metabolic dysfunction. Results: We identified and quantified 227 metabolites and 205 proteins in serum. Abnormalities indicating altered liver function, lipid dysregulation, and increased acute phase proteins were present in ID. In CSF, we measured 210 metabolites and 1,560 proteins with ID infants displaying metabolomic and proteomic changes indicating disrupted synaptogenesis. Concurrent systemic and CSF proteomic and metabolomic changes were present in the preanemic and anemic periods. Conclusions: Multiomic serum and CSF profiling uncovered pathways disrupted by ID in both the preanemic and anemic stages of infantile IDA, including evidence for liver metabolic dysfunction and acute phase responses. Parallel changes observed in serum and CSF potentially provide measurable serum biomarkers that reflect at-risk brain processes early during ID.
2022-03-18 | PXD028275 | Pride