Regulation of mRNA transcript expression by hypoxia in human peripheral blood lymphocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE7833 | GEO | 2007/05/18
SECONDARY ACCESSION(S): PRJNA100073
REPOSITORIES: GEO
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Project description:Microarray of whole blood maternal samples comparing the expression of genes in the maternal blood in pregnancies where the fetus was hypoxic at birth compared to those where the fetus was normoxic at birth. Intrapartum hypoxia is associated with severe neonatal morbidity and mortality. Current techniques to assess fetal hypoxic status during labour have a poor sensitivity. At birth, the lactate level in umbilical cord blood is used to assess the degree of fetal hypoxia during birth, such that a high lactate reflects a hypoxic fetus and a low lactate a normoxic fetus. We collected maternal blood prior to delivery and compared the expression of genes in the maternal blood in women delivering a normoxic or hypoxic fetus as evidenced by umbilcal cord blood levels.
2014-05-08 | E-MTAB-2054 | biostudies-arrayexpress
Project description:Intratumoral hypoxia causes the formation of dysfunctional blood vessels which contribute to tumor metastasis. Blood vessels are embedded in the tumor stroma where cancer-associated fibroblasts (CAFs) constitute the most prominent cellular component. We found that hypoxic human mammary CAFs promote blood vessel growth in CAF-endothelial cell co-cultures in vitro. Mass spectrometry-based proteomic analysis of CAF secretome unravels how hypoxic CAFs contribute to blood vessel abnormalities by altering the secretion of a multitude of pro- and anti-angiogenic factors. Hypoxia induces pronounced remodeling of the CAF proteome, including proteins that have not been previously related to this process. Amongst those, the uncharacterized antisense gene protein NCBP2-AS2 is one of the most transcriptionally upregulated proteins in the proteome and secretome of hypoxic CAFs. Silencing of NCBP2-AS2 abrogates the pro-angiogenic function acquired by hypoxic CAFs through decreasing VEGF expression levels to the levels found in normoxic CAFs.
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Project description:To understand hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic chemical hypoxic environment, for 2 weeks. Control, age-machted mice were maintained under normoxic conditions. Purpose: To examine and characterize the expression profile of genes expressed at chemical hypoxia of whole blood in comparison to the control. Methods: At the beginning of the experiment mice were divided into two groups, control (room condition) and chemical hypoxic (room condition). For conditioning, the chemical hypoxic group was supplemented with 200ng of CoCl2 per 100ml/day. Animalâs weight and food intake were monitored daily. Food and water were changed daily during the course of the experiment. Before and after the experiments the hematocrit was monitored by taking blood from the tail vein of control and hypoxic animals. After 15 days animals were euthanized using CO2 after whole blood extraction from V. Cava for further analysis. RNA from whole blood was isolated, processed and used for microarray-based expression profiling. Profiles were generated for genes differentially expressed at control versus chemical hypoxia in whole blood using a false discovery rate (FDR) of 0%.We validated the profiles by real-time quantitative reverse transcription-polymerase chain reaction (qPCR). Results: The regional transcriptomes associated with chemical hypoxia in whole blood were identified. We found 3094 genes that were differentially expressed in chemical hypoxic whole blood compared to control with a 0% FDR and a 2 fold cutoff. Conclusion: Transcriptome level differences exist between control and chemical hypoxia in whole blood. Our definition of the synaptic transcriptome provides insight into the functioning of the unique response to hypoxia in whole blood.
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Project description:To determine hypoxia mediated changes in whole blood, normal swiss webster mice were gradually exposed to a chronic hypobaric hypoxic environment up to 8500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic conditions in Kathmandu (c. 1300 mts above sea level). Purpose: To examine and characterize the expression profile of genes expressed at hypobaric hypoxia on Mt. Everest of whole blood in comparison to the control. Methods: At the beginning of the experiment mice were divided into two groups, control (room condition, Kathmandu, Nepal) and hypoxic (hypoxic condition). For conditioning, the hypoxic group was exposed to lower levels of hypobaric hypoxia during our mountaineering expedition to Mt Everest. The oxygen level was decreased according to our climbing protocol from 21% to about 7% over a period of 15 days. Food and water were changed daily during the course of the experiment. After 15 days animals were euthanized after whole blood extraction from V. Cava for further analysis. RNA from whole blood was isolated, processed and used for microarray-based expression profiling. Profiles were generated for genes differentially expressed at control versus hypobaric hypoxia in whole blood using a false discovery rate (FDR) of 0%.We validated the profiles by real-time quantitative reverse transcription-polymerase chain reaction (qPCR). Results: The regional transcriptomes associated with hypobaric hypoxia on Mt. Everest in whole blood were identified. We found 947 genes that were differentially expressed in normobaric hypoxic whole blood compared to control with a 0% FDR and a 2 fold cutoff. Conclusion: Transcriptome level differences exist between control and hypobaric hypoxia in whole blood. Our definition of the synaptic transcriptome provides insight into the functioning of the unique response to hypoxia in whole blood.
2010-05-07 | E-GEOD-15901 | biostudies-arrayexpress
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Project description:Hypoxic exposure during development can have a profound influence on offspring physiology, including cardiac dysfunction, yet many reptile embryos naturally experience periods of hypoxia in buried nests. American alligators experimentally exposed to developmental hypoxia demonstrate morphological and functional changes to the heart that persist into later life stages; however, the molecular bases of these changes remain unknown. We tested if targeted and persistent changes in steady-state protein expression underlie this hypoxic heart phenotype, using isobaric tags for relative and absolute quantitation (iTRAQ) proteomics. Alligator eggs were reared under normoxia or 10% hypoxia, then either sampled (embryo) or returned to normoxia for 2 years (juvenile). Three salient findings emerge from the integrated analysis of the 145 differentially expressed proteins in hypoxia-reared animals: (1) significant protein-protein interaction networks were identified only in up-regulated, indicating that the effects of developmental hypoxia are stimulatory and directed; (2) the up-regulated proteins substantially enriched processes related to protein turnover, cellular organization, and metabolic pathways, supporting increased resource allocation towards building and maintaining a higher functioning heart; and (3) the juvenile cardiac proteome retained many of the signature changes observed in embryonic hearts, supporting long-term reprogramming of cardiac myocytes induced by hypoxia during critical periods of development.
2019-05-22 | MSV000083838 | MassIVE