Control vs. Menopausal kidney cortex
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE20703 | GEO | 2010/09/14
SECONDARY ACCESSION(S): PRJNA129571
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression in kidney cortex of control mice and menopausal mice 8 weeks after mice entered menopause. Menopause was induced by injection of 4-vinylcyclohexene diepoxide. Samples = 12
2010-09-14 | E-GEOD-20703 | biostudies-arrayexpress
Project description:Gene expression in kidney cortex of diabetic mice and menopausal diabetic mice following 6 weeks of diabetes. Diabetes was induced with low-dose streptozotocin injections and menopause was induced by injection of 4-vinylcyclohexene diepoxide. Samples = 12
2010-09-14 | E-GEOD-20702 | biostudies-arrayexpress
Project description:Gene expression in kidney cortex of diabetic mice and menopausal diabetic mice following 6 weeks of diabetes. Diabetes was induced with low-dose streptozotocin injections and menopause was induced by injection of 4-vinylcyclohexene diepoxide.
2010-09-14 | GSE20702 | GEO
Project description:More women than men have died from heart disease over the last 20-25 years, with morbidity and mortality rising in women after menopause supported to be result of decreased circulating estrogen. Current literature lacks an understanding of the cellular and molecular mechanisms that capture the shift in susceptibility to cardiovascular disease (CVD) during the menopausal transition from pre- to peri- to menopause. Therefore, through use of a chemical model (4-vinylcyclohexene diepoxide; VCD) of ovarian failure, which allows us to preserve the peri-menopause state, we performed transcriptomic and proteomic analysis on post-mortem heart tissue. In general, pre-, peri-, and menopausal hearts clustered more closely (most similar) within each experimental group and perimenopausal hearts clustered more closely with premenopausal hearts than menopausal hearts (least similar). Both proteomes and transcriptomes showed similar trends in genes associated with atherothrombosis, contractility, and impaired nuclear signaling between pre-, peri-, and menopausal hearts. From this, we emphasized a menopause and angiotensin II (AngII) effect on AMP-activated protein kinase (AMPK) signaling and histone deacetylase (HDAC) activity where we found both an estrogen- and pathologic-dependent increase in phosphorylation of AMPK and decrease in class I HDAC activity. Additionally, we found a menopause-dependent decrease in class IIa HDAC activity and increase in class IIb activity. These findings suggest unique changes in pre-, peri-, and menopausal mice indicative of metabolic reprogramming and adverse cardiac remodeling with loss of estrogen.
2024-09-30 | GSE264423 | GEO
Project description:Menopause is associated with an increase in the prevalence and severity of hypertension in women. Although premenopausal females are protected against T cell-dependent immune activation and development of angiotensin II (Ang II) hypertension, this protection is lost in postmenopausal females. Therefore, the current study hypothesized that specific CD4+ T cell pathways are regulated by sex hormones and Ang II to mediate progression from premenopausal protection to postmenopausal hypertension. Menopause was induced in C57BL/6 mice via repeated 4-vinylcyclohexene diepoxide (VCD) injections, while premenopausal females received sesame oil vehicle. A subset of premenopausal mice and all menopausal mice were infused with Ang II for 14 days (Control, Ang II, Meno/Ang II). Proteomic and phosphoproteomic profiles of CD4+ T cells isolated from spleens were examined.Ang II markedly increased CD4+ T cell protein abundance and phosphorylation associated with DNA and histone methylation in both premenopausal and postmenopausal females. Compared to premenopausal T cells, Ang II infusion in menopausal mice increased T cell phosphorylation of MP2K2, an upstream regulator of ERK, and was associated with upregulated phosphorylation at ERK targeted sites. Additionally, Ang II infusion in menopausal mice decreased T cell phosphorylation of TLN1, a key regulator of IL-2R and FOXP3 expression. These findings identify novel, distinct intracellular T cell pathways that influence T cell-mediated inflammation during postmenopausal hypertension.
2021-09-09 | PXD021233 | Pride
Project description:This study was aimed at understanding the effects of menopause on knee osteoarthritis, specifically the cartilage proteome. Middle-aged female mice were randomized to receive intraperitoneal injections of either 4-vinylcyclohexene diepoxide (VCD) or sesame oil for 10 consecutive days. Through a serious of validation experiments, we and others have shown that VCD induces a menopausal phenotype, as evidenced by loss of estrus cyclicity and modification to sex hormone profiles. We also showed in our work that VCD injected mice present with more severe cartilage degeneration than sesame oil injected mice. Knee cartilage from the tibial plateau and femoral condyles were microdissected at mid-perimenopause (75 days after the first injection), start of menopause (115 days after the first injection), and late menopause (195 days after the first injection). These times points were chosen since cartilage pathology first presented in the VCD group, but not the sesame oil group, at the start of menopause. Cartilage samples were lyophilized and mass spectrometry proteomics were performed.
2023-06-01 | MSV000092077 | MassIVE
Project description:This SuperSeries is composed of the following subset Series: GSE20702: Diabetic vs. Menopausal/diabetic kidney cortex GSE20703: Control vs. Menopausal kidney cortex Refer to individual Series
2010-09-13 | E-GEOD-20704 | biostudies-arrayexpress
Project description:Mammalian females are born with a finite number of non-renewing primordial follicles, the majority of which remain in a quiescent state for many years. Due to their non-renewing nature, these “resting” oocytes are particularly vulnerable to xenobiotic insult, resulting in premature ovarian senescence and the formation of dysfunctional oocytes. In this study we characterised the mechanisms of ovotoxicity for three ovotoxic agents, 4-Vinylcyclohexene Diepoxide (VCD), Methoxychlor (MXC), and Menadione (MEN), all of which target immature follicles. Neonatal mouse ovaries (PND3-4) were cultured in the presence of 4-Vinylcyclohexene Diepoxide (50uM), Methoxychlor (50uM), and Menadione (5uM) for 96 hours to observe their effects on the ovarian transcriptome. This was done in the hopes of gaining a better understanding of the mechanisms underpinning xenobiotic induced pre-antral ovotoxicity.
2010-08-21 | GSE23725 | GEO
Project description:We produced new transcriptomic profiles of dementia-free human entorhinal cortex (n=99) and remodeled entorhinal cortex profiles from patients (n=64; Braak scores 0-6). There is a compelling link between menopause and Alzheimer's disease (AD), with few established molecular mechanisms. A lack of experimental models limits validation of causal drivers of these interactions. Here, we characterize the accelerated ovarian failure (OF) model of menopause in the triple-transgenic AD (3xTg-AD) mouse. Ovotoxin, 4-vinylcyclohexene diepoxide accelerated follicular loss, ablating circulating progesterone. OF resulted in decreased performance in the Y-maze, Novel Object Recognition, and Barnes Maze, consistent with accelerated AD. OF aggravated age-related impaired glucose tolerance and caused insulin resistance and these alterations correlated with the degree of cognitive impairment. Transcriptomic analyses of the mouse hippocampus identified 19 differentially regulated genes in OF mice, including some linked to AD, including C4b, Ifit3b, Cxcl13 and Gabrg2. Analyses of our 19 OF genes, identified that C4B expression was upregulated with both age and Braak score, while several revealed novel co-expression relationships, including between Shootin (SHTN1) and GABA receptor subunit (GABRG2). In summary, accelerated ovarian failure presents key cognitive, metabolic and molecular changes associated with age-related decline in cognitive function, indicating that it can be useful for the identification of novel therapeutic targets
2024-07-01 | GSE268659 | GEO
Project description:There is a compelling link between menopause and Alzheimer's disease (AD), with few established molecular mechanisms. A lack of experimental models limits validation of causal drivers of these interactions. Here, we characterize the accelerated ovarian failure (OF) model of menopause in the triple-transgenic AD (3xTg-AD) mouse. Ovotoxin, 4-vinylcyclohexene diepoxide accelerated follicular loss, ablating circulating progesterone. OF resulted in decreased performance in the Y-maze, Novel Object Recognition, and Barnes Maze, consistent with accelerated AD. OF aggravated age-related impaired glucose tolerance and caused insulin resistance and these alterations correlated with the degree of cognitive impairment. Transcriptomic analyses of the mouse hippocampus identified 19 differentially regulated genes in OF mice, including some linked to AD, including C4b, Ifit3b, Cxcl13 and Gabrg2. We produced new transcriptomic profiles of dementia-free human entorhinal cortex (n=99) and remodeled entorhinal cortex profiles from patients (n=64; Braak scores 0-6). Analyses of our 19 OF genes, identified that C4B expression was upregulated with both age and Braak score, while several revealed novel co-expression relationships, including between Shootin (SHTN1) and GABA receptor subunit (GABRG2). In summary, accelerated ovarian failure presents key cognitive, metabolic and molecular changes associated with age-related decline in cognitive function, indicating that it can be useful for the identification of novel therapeutic targets
2024-07-01 | GSE268557 | GEO