Hypothalamic expression differences between hypertensive BPH/2J and normotensive BPN/3J mouse strains
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Prof.Brian Morris
PROVIDER: E-GEOD-25076 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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.
2011-04-11 | GSE25076 | GEO
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: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 during circadian variations of blood pressure
| PRJNA135581 | ENA
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 âblood pressure highâ (BPH), normotensive âblood pressure normalâ (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. Animals: BPH/2J, BPL/1J and BPN/3J (142 ± 5 mmHg, 69 ± 1.7 mmHg, 94 ± 6 mmHg, SBP respectively) male mice (Jackson Laboratory) were maintained on a 12:12-h light-dark cycle and fed with standard chow ad libitum in facilities accredited by the Association for Assessment and Accreditation of Laboratory Animal Care. All procedures were in conformance with the National Research Council's Guide for the Care and Use of Laboratory Animals. Tissue collection: Mice (12 weeks old) were euthanized with CO2. Liver, heart, and kidney were flash frozen in liquid nitrogen. Aorta from the aortic root to the left renal artery was rinsed with PBS, immersed in 300ul of RNeasy Lysis buffer (Qiagen), and flash frozen in liquid nitrogen. RNA preparation: Tissues (~100mg, 5 mice per strain) were collected independently and homogenized in 2ml of Trizol (Invitrogen). After extraction with 0.4 ml of chloroform, RNA was extracted with SV Total RNA extraction kit (Promega) followed by DNase I treatment and purification using the RNeasy Kit (Qiagen). RNA was assayed for quality (Agilent Bioanalyzer) and yield (Ribogreen). Kidney, heart and liver RNA was amplified and labeled using a custom automated version of the RT/IVT protocol and reagents provided by Affymetrix. Aorta RNA was amplified and labeled using a custom automated version of the NuGEN Ovation WB protocol (NuGEN). Hybridization, labeling and scanning were according to Affymetrix. All samples were processed independently. Microarray analysis: Merck/Affymetrix mouse 1.0 custom arrays monitoring 38384 individual transcripts (25846 Entrez genes) were used. Raw intensity was normalized using the RMA algorithm.
2010-05-16 | E-GEOD-19817 | 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. 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: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
Project description:We examined if gene expression profiles differed between healthy (tumor-free) mice of strains that are known to have different pulmonary adenoma susceptibility (severity and frequency). Three females of 11 week old mice of 9 (129S1/SvlmJ, A/J, BALB/cJ, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, KK/HlJ, and MRL/MpJ) strains were selected for RNA extraction and hybridization on GeneChip® Mouse Gene 1.0 ST Arrays (Affymetrix, Santa Clara, CA). Each strain was compared to all other strains (36 unique comparisons total) to identify the most common differentially expressed probe sets among the population. The most common probesets were then compared between strain groups (increased vs. decreased spontaneous pulmonary adenoma frequency and severity).
2011-06-17 | E-GEOD-30015 | biostudies-arrayexpress
Project description:Respiratory viral infections follow an unpredictable clinical course in young children ranging from a common cold to respiratory failure. The transition from mild to severe disease occurs rapidly and is difficult to predict. The pathophysiology underlying disease severity has remained elusive. There is an urgent need to better understand the immune response in this disease to come up with biomarkers that may aid clinical decision making. In a prospective study, flow cytometric and genome-wide gene expression analyses were performed on blood samples of 26 children with a diagnosis of severe, moderate or mild Respiratory Syncytial Virus (RSV) infection. Differentially expressed genes were validated using Q-PCR in a second cohort of 80 children during three consecutive winter seasons. FACS analyses were also performed in the second cohort and on recovery samples of severe cases in the first cohort. Severe RSV infection was associated with a transient but marked decrease in CD4+ T, CD8+ T, and NK cells in peripheral blood. Gene expression analyses in both cohorts identified Olfactomedin4 (OLFM4) as a fully discriminative marker between children with mild and severe RSV infection, giving a PAM cross-validation error of 0%. Patients with an OLFM4 gene expression level above -7.5 were 6 times more likely to develop severe disease, after correction for age at hospitalization and gestational age. In conclusion, by combining genome-wide expression profiling of blood cell subsets with clinically well-annotated samples, OLFM4 was identified as a biomarker for severity of pediatric RSV infection. Samples were taken of 26 patients with acute RSV infections, divided into mild (n=9), moderate (n=9) and severe (n=8) disease. From moderate and severe diseased patients recovery samples were obtained as well.
2015-06-06 | E-GEOD-69606 | biostudies-arrayexpress