Mus musculus
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ABSTRACT:
PROVIDER: PRJNA135581 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identification of hypothalamic genes whose expression differs between active (peak of blood pressure) and inactive periods in the high blood pressure (BPH/2J) Schlager mouse, adjusted by their age- and activity-matched normal blood pressure (BPN/3J) controls using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. The whole hypothalamus was removed from BPH/2J and age-matched BPN/2J (n=3/group, 19 week old, ‘trough’ blood pressure) in the inactive period, when the blood pressure levels of the BPH/2J and BPN/3J models are similar. Hypothalamus of BPH/2J and age-matched BPN/2J (n=6/group, 26 week old, ‘peak’ blood pressure) were collected on the same way at the peak of the circadian variation, when there blood pressure difference between the strains was maximal. No pooling was performed. After extraction of RNA, cRNA was prepared and arrays performed using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays performed at the Ramaciotti Gene Function Analysis facility, University of New South Wales in Sydney, Australia.
2011-04-04 | E-GEOD-26007 | biostudies-arrayexpress
Project description:Identification of hypothalamic genes whose expression differs between high blood pressure (BPH/2J) and normal blood pressure (BPN/3J) Schlager mouse strains at age 6 weeks (young) and 26 weeks (mature) using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. The whole hypothalamus was removed from young (6-week-old) and adult (26-week-old) BPH/2J hypertensive mice and age-matched normotensive BPN/2J mice (n=6/group) at peak of 24 h blood pressure. No pooling was performed. After extraction of RNA, cRNA was prepared and arrays performed using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays at the Ramaciotti Gene Function Analysis facility, University of New South Wales in Sydney, Australia.
2011-04-11 | E-GEOD-25076 | biostudies-arrayexpress
Project description:Identification of hypothalamic genes whose expression differs between active (peak of blood pressure) and inactive periods in the high blood pressure (BPH/2J) Schlager mouse, adjusted by their age- and activity-matched normal blood pressure (BPN/3J) controls using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays.
2011-04-04 | GSE26007 | GEO
Project description:Identification of hypothalamic genes whose expression differs between high blood pressure (BPH/2J) and normal blood pressure (BPN/3J) Schlager mouse strains at age 6 weeks (young) and 26 weeks (mature) using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays.
2011-04-11 | GSE25076 | GEO
Project description:Aims: Hypertension poses a significant challenge to vasculature homeostasis and stands as the most common cardiovascular disease in the world. Its effects are especially profound on vasculature-lining endothelial cells that are directly exposed to the effects of excess pressure. Here, we characterize the in vivo transcriptomic response of cardiac endothelial cells to hypertension using the spontaneous hypertension mouse model BPH/2J. Methods and results: Verification of defective endothelial function in the BPH/2J hypertensive mouse strain was followed by acute isolation of cardiac endothelial cells and transcriptional profiling using RNA sequencing. Gene profiles from normotensive BPN/3J mice were compared to hypertensive animals. We observed over 3000 transcriptional differences between groups including pathways consistent with the cardiac fibrosis found in hypertensive animals. Importantly, many of the fibrosis-linked genes also differ between juvenile pre-hypertensive and adult hypertensive BPH/2J mice, suggesting that these transcriptional differences are hypertension-related. We also show that blood pressure normalization with amlodipine resulted in a subset of genes reversing their expression pattern, supporting the hypertension-dependency of altered gene expression. Yet, other transcripts were recalcitrant to therapeutic intervention illuminating the possibility that hypertension may irreversibly alter some endothelial transcriptional patterns. Conclusions: Hypertension has a profound effect on both function and transcription of endothelial cells, the latter of which was only partially restored with normalization of blood pressure. This study represents one of the first to quantify how endothelial cells are reprogrammed at the molecular level in cardiovascular pathology and advances our understanding of the transcriptional events associated with endothelial dysfunction.
2018-04-09 | GSE104530 | GEO
Project description:Hypothalamic expression differences between hypertensive BPH/2J and normotensive BPN/3J mouse strains
| PRJNA134743 | ENA
Project description:Small artery remodeling and endothelial dysfunction are hallmarks of hypertension. Evidence supports a likely causal association between cardiovascular diseases and endothelial-to-mesenchymal transition (EndMT), a cellular transdifferentiation process in which endothelial cells (ECs) partially lose their identity and acquire mesenchymal phenotypes. EC reprogramming represents an innovative strategy in regenerative medicine to prevent deleterious effects induced by cardiovascular diseases. We hypothesized that arteries from hypertensive mice present high levels of EndMT and that specific EC reprogramming can decrease blood pressure values and restore vascular function in resistance arteries in hypertensive mice. Here, we demonstrated OSK overexpression induced partial EC reprogramming in vitro, and these cells had lower migratory capability. Using spatial whole transcriptome atlas, we showed that OSK treatment of hypertensive BPH/2J mice attenuated EndMT and elastin breaks, and by other assays, we showed that OSK treatment reduced blood pressure and resistance arteries hypercontractility. OSK-treated hypertensive HAoECs showed high eNOS activation and NO production, with low ROS formation. Single-cell RNA analysis showed that OSK alleviated EC senescence and EndMT, restoring their phenotypes in HAoECs from hypertensive patients. Overall, these data indicate that OSK treatment and EC reprogramming can decrease blood pressure and reverse hypertension-induced vascular damage.
2025-08-26 | GSE298954 | GEO
Project description:Analysis of kidneys from 12 week BPH/2J hypertensive and age matched normotensive BPN/3J controls - males and females. The results provide insights into the genes that are involved in hypertension in both males and females, as well as highlight mechanisms that underlye sex differences in hypertension. We show that female data can be used to refine candidate genes and pathways, as well as highlight potential mechanisms to explain the differences in prevalence and severity of disease between the sexes. Male and female kidneys from 12 week old hypertensive (BPH/2J) and normotensive (BPN/3J) mice were collected for RNA extraction and hybridization on Affymetrix microarrays. We used data obtained from male and female kidneys to identify common genes that are involved in the development of hypertension in males and females
2014-09-28 | E-GEOD-54015 | biostudies-arrayexpress
Project description:Analysis of kidneys from 12 week BPH/2J hypertensive and age matched normotensive BPN/3J controls - males and females. The results provide insights into the genes that are involved in hypertension in both males and females, as well as highlight mechanisms that underlye sex differences in hypertension. We show that female data can be used to refine candidate genes and pathways, as well as highlight potential mechanisms to explain the differences in prevalence and severity of disease between the sexes.
2014-09-28 | GSE54015 | GEO
Project description:Hypertension is a condition with major cardiovascular and renal complications, affecting nearly a billion patients worldwide. Few validated gene targets are available for pharmacological intervention, so there is a need to identify new biological pathways regulating blood pressure and containing novel targets for treatment. The genetically hypertensive “blood pressure high” (BPH), normotensive “blood pressure normal” (BPN), and hypotensive "blood pressure low" (BPL) inbred mouse strains are an ideal system to study differences in gene expression patterns that may represent such biological pathways. We profiled gene expression in liver, heart, kidney, and aorta from BPH, BPN, and BPL mice and determined which biological processes are enriched in observed organ-specific gene signatures. As a result, we identified multiple biological pathways linked to blood pressure phenotype that could serve as a source of candidate genes causal for hypertension. In order to distinguish causal genes from responsive genes in the kidney gene signature we integrated phenotype associated genes into Genetic Bayesian networks, identifying several novel candidate genes causal for hypertension. The integration of data from gene expression profiling and genetics networks is a valuable approach to identify novel potential targets for the pharmacological treatment of hypertension.
2010-01-12 | GSE19817 | GEO