Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA98753 | ENA |
REPOSITORIES: ENA
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Project description:Dysregulation of the circulating and tissue-based renin-angiotensin system in preeclampsia
| PRJNA98753 | ENA
Project description:Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps. In this study we analyzed the renin-angiotensin system in adipose tissue, decidua and placenta from women with uneventful pregnancy and women with preeclampsia. We also analyzed the tissue by Affymetrix chips in a comparison study (control vs. preeclampsia) Experiment Overall Design: 6 affymetrix human expression chips (GPL570) were analyzed. Experiment Overall Design: They represent 3 tissues (pooled from 10 individuals each) from patients with preeclampsia and from patients with uneventful pregnancy (collected by cesaraen section). Tissues from patients with uneventful pregnancy are the controls in comparison to tissues of patients with preeclampsia.
2008-06-14 | E-GEOD-6573 | biostudies-arrayexpress
Project description:The brain renin-angiotensin system (RAS) stimulates resting metabolic rate in part through a mechanism involving suppression of the circulating RAS. This effect appears to be mediated through a reduction in angiotensin AT2 receptor (AT2R) signaling within inguinal fat. To examine the molecular mechanisms underlying this effect, mice with hyperactivity of the brain RAS (“sRA” mice, expressing human renin via the synapsin promoter and human angiotensinogen via its own promoter) and littermate controls were chronically infused with vehicle or the AT2R specific agonist, CGP-42112a (CGP, 90 ng/hr, 8 wk, sc). To identify altered signaling pathways, total RNA was isolated from inguinal adipose tissue and transcript abundance was quantitated by RNA-Seq.
2016-12-07 | GSE77214 | GEO
Project description:Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps. In this study we analyzed the renin-angiotensin system in adipose tissue, decidua and placenta from women with uneventful pregnancy and women with preeclampsia. We also analyzed the tissue by Affymetrix chips in a comparison study (control vs. preeclampsia) Keywords: disease comparison, disease state
2007-01-01 | GSE6573 | GEO
Project description:The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage. This is a comparison between the renin inhibitor aliskiren with the At1 antagonist losartan in mice with chronic kidney disease due to renal ablation. Renal tissue from ablated mice was used after 6-week treatment with either 500 mg/l losartan or 50 mg/kg aliskiren per day (n = 5)
2012-11-05 | E-GEOD-34552 | biostudies-arrayexpress
Project description:LC-MS/MS Proteomics was performed to determine proteomic differences between colon adenocarcinoma (CA) tissues and patient-matched normal colon tissues, CA-derived primary cell lines and NC-derived primary cells, and between LGCA tissues and cell lines and HGCA tissues and cell lines. Biological processes which may link the renin-angiotensin system and CA were investigated, revealing enrichment of various signalling pathways that may play roles in CA onset and progression directly or via the renin-angiotensin system.
2022-08-12 | PXD024449 | Pride
Project description:The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage. This is a comparison between the renin inhibitor aliskiren with the At1 antagonist losartan in mice with chronic kidney disease due to renal ablation.
2012-11-05 | GSE34552 | GEO
Project description:Severe preeclampsia: new blood circulating biomarkers
| PRJNA212688 | ENA
Project description:High blood pressure is one of the major public health problems which causes severe disorders in several tissues including the human kidney. One of the most important signaling pathways associated with the regulation of blood pressure is the renin-angiotensin system (RAS), with its main mediator angiotensin II (ANGII). Elevated levels of circulating and intracellular ANGII and aldosterone lead to pro-fibrotic, -inflammatory and -hypertrophic milieu that causes remodelling and dysfunction in cardiovascular and renal tissues. Furthermore, ANGII has been recognized as major risk factor for the induction of apoptosis in podocytes, ultimately leading to chronic kidney disease (CKD). In the past, disease modeling of kidney-associated malignancies was extremely difficult, as the derivation of kidney originated cells is very challenging. Here we describe a differentiation protocol for reproducible differentiation of SIX2-positive urine derived renal progenitor cells (UdRPCs) into mature podocytes bearing typical foot processes. The UdRPCs-derived podocytes show the ability to execute Albumin endocytosis and the activation of the renin-angiotensin system by being responsive to ANGII stimulation. Our data reveals the ANGII dependent downregulation of NPHS1 and SYNPO, resulting in the disruption of the complex podocyte cytoskeletal architecture, as shown by immunofluorescence-based detection of α–ACTININ. In the present manuscript we confirm and propose UdRPCs as a unique cell type useful for studying nephrogenesis and associated diseases. Furthermore, the responsiveness of UdRPCs-derived podocytes to ANGII implies potential applications in nephrotoxicity studies and drug screening.
2022-03-31 | GSE171240 | GEO
Project description:We aim to identify the role of Renin Angiotensin pathway by identifying novel genes and microRNAs altered by overexpressing angiotensiogen specifcally in the adipose tissue
2020-07-15 | GSE147935 | GEO