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Expression data from Human Kidney (HK) samples

ABSTRACT: Males are 50% more likely to develop end stage kidney failure compared to women. In this study we wanted to find out the molecular mechanism responsible for this increased risk. We collected kidney samples from patients with and without kidney disease and performed a comprehensive gene expression analysis in healthy and diseased male and female kidneys. Interestingly, the set of gender biased genes in healthy kidneys were different from those in diseased kidneys indicating not only baseline gene expression differences but also that the male and female kidney respond differently to disease condition. Our studies indicate that men and women with kidney problems might need to be treated differently. Keywords: Gender difference

ORGANISM(S): Homo sapiens

PROVIDER: GSE12682 | GEO | 2010/04/13

SECONDARY ACCESSION(S): PRJNA112681

REPOSITORIES: GEO

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Expression data from Human Kidney (HK) samples

Project description:Males are 50% more likely to develop end stage kidney failure compared to women. In this study we wanted to find out the molecular mechanism responsible for this increased risk. We collected kidney samples from patients with and without kidney disease and performed a comprehensive gene expression analysis in healthy and diseased male and female kidneys. Interestingly, the set of gender biased genes in healthy kidneys were different from those in diseased kidneys indicating not only baseline gene expression differences but also that the male and female kidney respond differently to disease condition. Our studies indicate that men and women with kidney problems might need to be treated differently. Keywords: Gender difference We collected 42 kidney samples from healthy living transplant donors, nephrectomies and from diagnostic kidney biopsies. Preliminary studies did not show significant gene expression differences in control kidneys based on the collection method (i.e. living kidney biopsy vs. unaffected portion of tumor nephrectomy). We grouped the tissue samples based on the histological readings of the kidney biopsies. Samples with evidence of glomerular and tubulointerstitial fibrosis were assigned into the diseased group. Characteristics of the research participants indicate diverse ethnic and disease groups and mild (StageIII) CKD. The tissue was microdissected into glomerular and tubulointerstitial fractions and expression arrays were performed separately.

2010-04-13 | E-GEOD-12682 | biostudies-arrayexpress

Expression data from Balb/c mice kidney samples

2009-12-01 | GSE12683 | GEO

Expression data from Balb/c mice kidney samples

Project description:Males are 50% more likely to develop end stage kidney failure compared to women. As a model of the human condition we analyzed gene expression changes in healthy and diseased mouse kidneys. Interestingly, the set of gender biased genes in healthy kidneys were different from those in diseased kidneys indicating not only baseline gene expression differences but also that the male and female kidney respond differently to disease condition. Keywords: Gender difference We used AffymetrixM430A2.0 microarrays to determine global gene expression differences in kidneys of 10-week old healthy Balb/c male and female mice. In order to identify gene expression differences under disease conditions, animals were injected with doxorubicin, a substance that is known to induce albuminuria and glomerulosclerosis in Balb/c mice as it is directly toxic to podocytes.

2010-03-03 | E-GEOD-12683 | biostudies-arrayexpress

Watanabe2018_Simple markov model

Project description:Simple Markov model. There are 3 disease states: Healthy, Sick, and Dead, where the Dead state is terminal. The yearly transition probabilities are: Healthy to Dead: 0.01; Healthy to Sick: 0.2 for Male and 0.1 for Female; Sick to Healthy: 0.1; Sick to Dead: 0.3. The transition probability now depends on the cohort (Male or Female) and can be expressed as a function of a Boolean covariate Male. Initial conditions: Healthy = (50 Male, 50 Female), Sick = (0,0) and Dead = (0,0). Output: Number of men and women in each disease state for years 1-10.

2019-01-30 | MODEL1803120004 | BioModels

Watanabe2018_State transition model dependent on changing parameters

Project description:Model dependent on changing parameters. There are 3 disease states: Healthy, Sick, and Dead, where the Dead state is terminal. The yearly transition probabilities are: Healthy to Dead: Age/1000; Healthy to Sick: according to function F1 depending on Age and Male parameters; Sick to Healthy: 0.1; Sick to Dead: according to function F2 depending on Age and Male parameters. Pre-Transition Rules: Age increased by 1 each cycle. Initial conditions: Healthy = (50 Male, 50 Female with Age =1,2,…,50 for each individual), Sick = (0,0) and Dead = (0,0). Output: Number of men and women in each disease state for years 1-10 and their ages in each state.

2019-01-30 | MODEL1803120005 | BioModels

Watanabe2018_State Transition Model with Treatment and Costs

Project description:Model with functions depending on Age, Male, BP (Blood Pressure). There are 3 disease states: Healthy, Sick, and Dead, where the Dead state is terminal. The yearly transition probabilities are: Healthy to Dead: Age/1000; Healthy to Sick: According to function F1 depending on Age and Male and BP; Sick to Healthy: 0.1; Sick to Dead: according to function F2 depending on Age and Male. Pre-Transition Rules: Age increased by 1 and BP by Age/10 each simulation cycle. Post-Transition Rules: Treatment = BP>140 , becomes 1 when BP crosses 140 threshold; BP =BP-Treatment*10 , meaning a drop of 10 once treatment is applied; CostThisYear = Age + \Treatment*10 , cost depends on age and if treatment was taken; Cost= Cost + CostThisYear , it accumulates cost over time. Initial conditions: Healthy = (50 Male, 50 Female with Age =1,2,...,50 for each individual), BP =120, Sick = (0,0) and Dead = (0,0). Output: Number of men and women in each disease state for years 1-10 and their ages and costs in each state. A stratified report by male and female and young – up to age 30 and old above age 30 is produced.

2019-01-30 | MODEL1803120006 | BioModels

Hypertensive Rat Kidney Study: Gender-Selective Responses to Salt in Dahl-Iwai & Sprague-Dawley Rats

Project description:Dahl-Iwai (DI) salt-sensitive rats were studied using microarrays to identify gender-specific differences in the kidney, both basal differences and responses to a high salt diet. In DI rat kidneys, gene expression profiles demonstrated inflammatory and fibrotic responses selectively in females. Gonadectomy of DI rats abrogated gender differences in gene expression. Gonadectomized female and gonadectomized male DI rats both responded to high salt with the same spectrum of gene expression changes as intact female DI rats. Androgens dominated the gender selective responses to salt. Several androgen-responsive genes were identified with roles potentiating the differential responses to salt including increased male expression of Angiotensin-Vasopressin Receptor and Prolactin Receptor, decreased 5-alpha reductase, and mixed increases and decreases in expression of Cyp4a- genes that can produce eicosanoid hormones. These gender differences potentiate sodium retention by males, and increase kidney function during gestation by females. Keywords: Disease-State Analysis (Salt-Sensitive Hypertension)

2007-07-01 | GSE5285 | GEO

Transcription profiling of rat model of hypertension kidney reveals gender-selective responses to salt in Dahl-Iwai and Sprague-Dawley strains

Project description:Dahl-Iwai (DI) salt-sensitive rats were studied using microarrays to identify gender-specific differences in the kidney, both basal differences and responses to a high salt diet. In DI rat kidneys, gene expression profiles demonstrated inflammatory and fibrotic responses selectively in females. Gonadectomy of DI rats abrogated gender differences in gene expression. Gonadectomized female and gonadectomized male DI rats both responded to high salt with the same spectrum of gene expression changes as intact female DI rats. Androgens dominated the gender selective responses to salt. Several androgen-responsive genes were identified with roles potentiating the differential responses to salt including increased male expression of Angiotensin-Vasopressin Receptor and Prolactin Receptor, decreased 5-alpha reductase, and mixed increases and decreases in expression of Cyp4a- genes that can produce eicosanoid hormones. These gender differences potentiate sodium retention by males, and increase kidney function during gestation by females. Experiment Overall Design: - 68 samples/rats/data tables are represented. Experiment Overall Design: - One microarray was used for each sample. Experiment Overall Design: - 3 rat

2008-06-13 | E-GEOD-5285 | biostudies-arrayexpress

Expression data from kidney of 36d old PKD/Mhm rats.

Project description:Gender has strong impact on kidney performance. Female gender tends to be renal protective. PKD/Mhm is rat model for human polycystic kidney disease (PKD) caused by a mutation in gene Anks6. PKD progresses faster in male rats compared with females. We used microarrays to detect gender-dependent gene expression in kidney of 36d old PKD/Mhm rats. Keywords: gender, genotype

2009-09-30 | GSE13065 | GEO

LC-MS of PBMC in SLE and healthy control

Project description:Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease that displays a significant gender difference in terms of incidence and severity. However, the underlying mechanisms accounting for sexual dimorphism remain unclear. To reveal the heterogeneity in the pathogenesis of SLE between male and female patients. PBMC were collected from 15 patients with SLE (7 males, 8 females) and 15 age-matched healthy controls (7 males, 8 females) for proteomic analysis. Enrichment analysis of proteomic data revealed that type I interferon signaling and neutrophil activation networks mapped to both male and female SLE, while male SLE has a higher level of neutrophil activation compared with female SLE. Our findings define gender heterogeneity in the pathogenesis of SLE and may facilitate the development of gender-specific treatments.

2022-08-12 | PXD033144 | Pride

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