Browse
Submit Data
Databases
API
Help

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases.

ABSTRACT: Epidemiological studies of blood pressure in men and women and in experimental animal models point to substantial sex differences in the occurrence of arterial hypertension as well as in the various manifestations of arterial hypertension, including myocardial infarction, stroke, retinopathy, chronic kidney failure, as well as hypertension-associated diseases (e.g. diabetes mellitus). Increasing evidence demonstrates that the endothelin (ET) system is a major player in the genesis of sex differences in cardiovascular and renal physiology and diseases. Sex differences in the ET system have been described in the vasculature, heart and kidney of humans and experimental animals. In the current review, we briefly describe the role of the ET system in the cardiovascular and renal systems. We also update information on sex differences at different levels of the ET system including synthesis, circulating and tissue levels, receptors, signaling pathways, ET actions, and responses to antagonists in different organs that contribute to blood pressure regulation. Knowledge of the mechanisms underlying sex differences in arterial hypertension can impact therapeutic strategies. Sex-targeted and/or sex-tailored approaches may improve treatment of cardiovascular and renal diseases.

SUBMITTER: Gohar EY

PROVIDER: S-EPMC4992599 | biostudies-other | 2016 Aug

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

GPCRs in context: sexual dimorphism in the cardiovascular system.

Project description:Cardiovascular disease (CVD) remains the largest cause of mortality worldwide, and there is a clear gender gap in disease occurrence, with men being predisposed to earlier onset of CVD, including atherosclerosis and hypertension, relative to women. Oestrogen may be a driving factor for female-specific cardioprotection, though androgens and sex chromosomes are also likely to contribute to sexual dimorphism in the cardiovascular system (CVS). Many GPCR-mediated processes are involved in cardiovascular homeostasis, and some exhibit clear sex divergence. Here, we focus on the G protein-coupled oestrogen receptor, endothelin receptors ETA and ETB and the eicosanoid G protein-coupled receptors (GPCRs), discussing the evidence and potential mechanisms leading to gender dimorphic responses in the vasculature. The use of animal models and pharmacological tools has been essential to understanding the role of these receptors in the CVS and will be key to further delineating their sex-specific effects. Ultimately, this may illuminate wider sex differences in cardiovascular pathology and physiology. LINKED ARTICLES:This article is part of a themed section on Molecular Pharmacology of GPCRs. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.21/issuetoc.

| S-EPMC6177612 | biostudies-literature

Sexual-dimorphism in human immune system aging.

Project description:Differences in immune function and responses contribute to health- and life-span disparities between sexes. However, the role of sex in immune system aging is not well understood. Here, we characterize peripheral blood mononuclear cells from 172 healthy adults 22-93 years of age using ATAC-seq, RNA-seq, and flow cytometry. These data reveal a shared epigenomic signature of aging including declining naïve T cell and increasing monocyte and cytotoxic cell functions. These changes are greater in magnitude in men and accompanied by a male-specific decline in B-cell specific loci. Age-related epigenomic changes first spike around late-thirties with similar timing and magnitude between sexes, whereas the second spike is earlier and stronger in men. Unexpectedly, genomic differences between sexes increase after age 65, with men having higher innate and pro-inflammatory activity and lower adaptive activity. Impact of age and sex on immune phenotypes can be visualized at https://immune-aging.jax.org to provide insights into future studies.

| S-EPMC7005316 | biostudies-literature

ImmGen report: sexual dimorphism in the immune system transcriptome.

Project description:Sexual dimorphism in the mammalian immune system is manifested as more frequent and severe infectious diseases in males and, on the other hand, higher rates of autoimmune disease in females, yet insights underlying those differences are still lacking. Here we characterize sex differences in the immune system by RNA and ATAC sequence profiling of untreated and interferon-induced immune cell types in male and female mice. We detect very few differentially expressed genes between male and female immune cells except in macrophages from three different tissues. Accordingly, very few genomic regions display differences in accessibility between sexes. Transcriptional sexual dimorphism in macrophages is mediated by genes of innate immune pathways, and increases after interferon stimulation. Thus, the stronger immune response of females may be due to more activated innate immune pathways prior to pathogen invasion.

| S-EPMC6754408 | biostudies-literature

Estrogen-mediated downregulation of AIRE influences sexual dimorphism in autoimmune diseases.

Project description:Autoimmune diseases affect 5% to 8% of the population, and females are more susceptible to these diseases than males. Here, we analyzed human thymic transcriptome and revealed sex-associated differences in the expression of tissue-specific antigens that are controlled by the autoimmune regulator (AIRE), a key factor in central tolerance. We hypothesized that the level of AIRE is linked to sexual dimorphism susceptibility to autoimmune diseases. In human and mouse thymus, females expressed less AIRE (mRNA and protein) than males after puberty. These results were confirmed in purified murine thymic epithelial cells (TECs). We also demonstrated that AIRE expression is related to sexual hormones, as male castration decreased AIRE thymic expression and estrogen receptor ?-deficient mice did not show a sex disparity for AIRE expression. Moreover, estrogen treatment resulted in downregulation of AIRE expression in cultured human TECs, human thymic tissue grafted to immunodeficient mice, and murine fetal thymus organ cultures. AIRE levels in human thymus grafted in immunodeficient mice depended upon the sex of the recipient. Estrogen also upregulated the number of methylated CpG sites in the AIRE promoter. Together, our results indicate that in females, estrogen induces epigenetic changes in the AIRE gene, leading to reduced AIRE expression under a threshold that increases female susceptibility to autoimmune diseases.

| S-EPMC4811157 | biostudies-literature

Circular RNAs in Rat Models of Cardiovascular and Renal diseases

Project description:The objective of this study was to profile circular RNAs (circRNAs) in rat genetic models of cardiovascular and renal disease. Renal profiles were obtained from the Dahl Salt-Sensitive rat (S), the Dahl Salt-Resistant rat (R), the Spontaneously Hypertensive Rat (SHR) and the Wistar Kyoto rat (WKY).

2017-07-27 | GSE92669 | GEO

Orphan receptor GPR37L1 contributes to the sexual dimorphism of central cardiovascular control.

Project description:BACKGROUND:Over 100 mammalian G protein-coupled receptors are yet to be matched with endogenous ligands; these so-called orphans are prospective drug targets for the treatment of disease. GPR37L1 is one such orphan, abundant in the brain and detectable as mRNA in the heart and kidney. GPR37L1 ablation was reported to cause hypertension and left ventricular hypertrophy, and thus, we sought to further define the role of GPR37L1 in blood pressure homeostasis. METHODS:We investigated the cardiovascular effects of GPR37L1 using wild-type (GPR37L1wt/wt) and null (GPR37L1KO/KO) mice established on a C57BL/6J background, both under baseline conditions and during AngII infusion. We profiled GPR37L1 tissue expression, examining the endogenous receptor by immunoblotting and a ?-galactosidase reporter mouse by immunohistochemistry. RESULTS:GPR37L1 protein was abundant in the brain but not detectable in the heart and kidney. We measured blood pressure in GPR37L1wt/wt and GPR37L1KO/KO mice and found that deletion of GPR37L1 causes a female-specific increase in systolic, diastolic, and mean arterial pressures. When challenged with short-term AngII infusion, only male GPR37L1KO/KO mice developed exacerbated left ventricular hypertrophy and evidence of heart failure, while the female GPR37L1KO/KO mice were protected from cardiac fibrosis. CONCLUSIONS:Despite its absence in the heart and kidney, GPR37L1 regulates baseline blood pressure in female mice and is crucial for cardiovascular compensatory responses in males. The expression of GPR37L1 in the brain, yet absence from peripheral cardiovascular tissues, suggests this orphan receptor is a hitherto unknown contributor to central cardiovascular control.

| S-EPMC5889568 | biostudies-literature

Sexual dimorphism in human immune system aging

Project description:Sexual dimorphism in human immune system aging

| PRJNA591038 | ENA

Sexual dimorphism in human immune system aging

Project description:Sexual dimorphism in human immune system aging

| PRJNA591039 | ENA

Sexual dimorphism in immune function and oxidative physiology across birds: The role of sexual selection.

Project description:Sex-specific physiology is commonly reported in animals, often indicating lower immune indices and higher oxidative stress in males than in females. Sexual selection is argued to explain these differences, but empirical evidence is limited. Here, we explore sex differences in immunity, oxidative physiology and packed cell volume of wild, adult, breeding birds (97 species, 1997 individuals, 14 230 physiological measurements). We show that higher female immune indices are most common across birds (when bias is present), but oxidative physiology shows no general sex-bias and packed cell volume is generally male-biased. In contrast with predictions based on sexual selection, male-biased sexual size dimorphism is associated with male-biased immune measures. Sexual dichromatism, mating system and parental roles had no effect on sex-specificity in physiology. Importantly, female-biased immunity remained after accounting for sexual selection indices. We conclude that cross-species differences in physiological sex-bias are largely unrelated to sexual selection and alternative explanations should be explored.

| S-EPMC9305230 | biostudies-literature

Sexual size dimorphism in anurans: roles of mating system and habitat types.

Project description:BackgroundSexual size dimorphism (SSD) is widespread and variable among animals. Sexual selection, fecundity selection and ecological divergence between males and females are the major evolutionary forces of SSD. However, the influences of mating system and habitat types on SSD have received little attention. Here, using phylogenetic comparative methods, we at first examine the hypotheses to that mating system (intensity of sexual selection) and habitat types affect significantly variation in SSD in anurans (39 species and 18 genera).ResultsOur data set encompass 39 species with female-biased SSD. We provide evidence that the effects of mating system and habitat types on SSD were non-significant across species, also when the analyses were phylogenetically corrected.ConclusionsContrast to the hypotheses, our findings suggest that mating system and habitat types do not play an important role in shaping macro-evolutionary patterns of SSD in anurans. Mating system and habitat types cannot explain the variation in SSD when correcting for phylogenetic effects.

| S-EPMC3879228 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data