This SuperSeries is composed of the SubSeries listed below.
Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve.
Age, Specimen part, Treatment
View SamplesThe transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression.
Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.
Specimen part, Cell line
View SamplesSpaceflight results in a number of adaptations to skeletal muscle, including atrophy and shifts towards faster muscle fiber types. To identify changes in gene expression that may underlie these adaptations, microarray expression analysis was performed on gastrocnemius from mice flown on the STS-108 shuttle flight (11 days, 19 hours) versus mice maintained on earth for the same period. Additionally, to identify changes that were due to unloading and reloading, microarray analyses were conducted on calf muscle from ground-based mice subjected to hindlimb suspension (12 days) and mice subjected to hindlimb suspension plus a brief period of reloading (3.5 hours) to simulate the time between landing and sacrifice of the spaceflight mice.
Effects of spaceflight on murine skeletal muscle gene expression.
No sample metadata fields
View SamplesPluripotent P19CL6 embryonic carcinoma cells can be differentiated to a cardiac lineage by culture in the presence of DMSO. The goal of this study was to characterize temporal gene expression patterns associated with cardiogenic differentiation. Gene expression analysis was conducted on differentiating P19CL6 cells at several time points following induction with 1% DMSO. Samples were processed for analysis by Affymetrix GeneChip.
Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.
Cell line
View SamplesMyelinating glia in the auditory system enclose auditory nerve fibers, providing an insulating effect that facilitates rapid transfer of auditory information from the ear to the brain. Here we show that noise exposure at the levels sufficient for inducing hearing loss cause a rapid cellular and molecular response on myelinating glia that precedes neuron degeneration. The response is characterized by inflammatory response, myelin dysmorphology and widespread changes in myelin-related gene expression. Another characteristic was change in expression of the quaking gene (QKI), which encodes a group of RNA binding proteins that are enriched in myelinating glia. Changes in QKI were accompanied by changes in numerous known and potential QKI target genes, including many genes associated with myelination. Our results implicate QKI as a critical early component in the noise response, influencing glia dysfunction that leads to auditory nerve demyelination and, ultimately, sensorineural hearing loss.
Noise-induced dysregulation of <i>Quaking</i> RNA binding proteins contributes to auditory nerve demyelination and hearing loss.
Sex, Specimen part, Time
View SamplesSpiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves.
Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve.
Specimen part
View SamplesSpiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves.
Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve.
Specimen part
View SamplesArterial smooth muscle cells (ASMCs) undergo phenotypic changes during development and pathological processes in vivo and during cell culture in vitro. Our previous studies demonstrated that retrovirally-mediated expression of the versican V3 splice variant (V3) that lacks glycosaminoglycan chains by ASMCs retards cell proliferation and migration in vitro and reduces neointimal thickening, macrophage and lipid accumulation in animal models of vascular injury and atherosclerosis. However, the molecular pathways induced by V3 expression that are responsible for these changes are not yet clear. In the present study, we employed a microarray approach to examine how expression of V3 induced changes in gene expression and the molecular pathways in ASMCs. We found that forced expression of V3 by ASMCs affected expression of 521 genes by more than 1.5 fold. Gene ontology (GO) analysis shows that components of extracellular matrix were the most significantly affected by V3 expression, indicating that V3 expression elicits profound remodeling of extracellular matrix. In addition, genes regulating the formation of the cytoskeleton which also serve as markers of contractile smooth muscle cells were significantly upregulated. On the other hand, components of the complement system, chemokines, chemokine receptors, and transcription factors crucial for regulating inflammatory processes were among the genes most downregulated. Consistently, we found that the level of myocardin, a key transcription factor promoting contractile ASMC phenotype, was greatly increased while proinflammatory transcription factors NFkappaB1 and C/EBP were significantly attenuated in V3-expressing SMCs. Such results indicate that V3 expression reprograms ASMC into differentiated and anti-inflammatory phenotypes. Overall, these findings demonstrate that expression of V3 reprograms ASMCs promoting anti-inflammatory and differentiated smooth muscle cell phenotypes potentially by altering cell-ECM interaction and focal adhesion signaling pathways.
Expression of V3 Versican by Rat Arterial Smooth Muscle Cells Promotes Differentiated and Anti-inflammatory Phenotypes.
Specimen part
View SamplesSpiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves.
Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve.
Age, Specimen part, Treatment
View SamplesThis study was conducted to examine normal gene expression in the pharyngeal arch during mouse embryonic development
No associated publication
Specimen part
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