Transcriptomic profiling (RNA-seq) of lung endothelial cells from wild-type (WT) and TET2KO mice following 28 days of Angiotensin II treatment.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE342961 | GEO | 2026/08/10
REPOSITORIES: GEO
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Project description:Chronic Angiotensin II (Ang II) infusion is a known inducer of cardiac remodeling, hypertrophy, and fibrosis, processes that are intricately linked to endothelial dysfunction. To determine how endothelial-specific deletion of TET2 affects the cardiac microenvironment under stress, we performed total RNA sequencing (RNA-seq) on the mid-ventricular region of the heart harvested from wild-type (WT) and endothelial-specific TET2 knockout (TET2KO) mice after 28 days of Ang II infusion. This dataset captures the global transcriptomic landscape of the heart, facilitating the identification of gene expression shifts, extracellular matrix remodeling, and hypertrophic markers associated with endothelial TET2 deficiency.
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Project description:Here we evaluated the contribution of cellular senescence to the effect of chronic exposure to low dose angiotensin II in a mouse model that mimics the initiation of hypertension. We utilized the INK-ATTAC (p16ink4a - Apoptosis Through Targeted Activation of Caspase 8) mouse model that allows for conditional elimination of p16ink4a -dependent senescent cells by administration of AP20187. INK-ATTAC mice received continuous low doses of angiotensin II over 3 weeks and AP20187 vs vehicle. In the kidneys increased expression of ATM, p15 and p21 matched with angiotensin II induction of senescence-associated secretory phenotype genes MMP3, FGF2, IGFBP2, and tPA. AP20187-mediated elimination of p16-dependent senescent cells prevented physiologic, cellular and molecular responses to angiotensin II. We conclude that angiotensin II induces a relatively selective senescence transformation of renal endothelial cells that could provide a novel therapeutic target for senolytic drugs as alternative treatment options for hypertension and resulting tissue damage.
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Project description:In order to characterize gene expression networks linked to AT1 angiotensin receptors in the kidney, we carried out genome-wide transcriptional analysis of RNA from kidneys of wild-type (WT) and AT1A receptor-deficient mice (KOs) at baseline and after 2 days of angiotensin II infusion (1 ug/kg/min), using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays. At baseline, 405 genes were differentially expressed (>1.5X) between WT and KO kidneys. Of these, more than 80% were up-regulated in the KO group including genes involved in inflammation, oxidative stress, and cell proliferation. After 2 days of angiotensin II infusion in WT mice, expression of ~805 genes was altered (18% up-regulated, 82% repressed). Genes in metabolism and ion transport pathways were up-regulated while there was attenuated expression of protective genes against oxidative stress including glutathione synthetase and mitochondrial SOD2. Angiotensin II infusion has little effect on blood pressure in KOs. Nonetheless, expression of more than 250 genes was altered in kidneys from KO mice during angiotensin II infusion; 14% were up-regulated, while 86% were repressed including genes involved in immune responses, angiogenesis, and glutathione metabolism. Between WT and KO kidneys during angiotensin II infusion, 728 genes were differentially expressed; 10% were increased and 90% were decreased in the WT group. Differentially regulated pathways included those involved in ion transport, immune responses, metabolism, apoptosis, cell proliferation, and oxidative stress. This genome-wide assessment should facilitate identification of critical distal pathways linked to blood pressure regulation. To define gene expression patterns in kidney triggered by of activation AT1 receptors, we used genome-wide transcriptional analysis of RNA from kidneys of wild-type and AT1A receptor-deficient mice at baseline and after 2 days of angiotensin II infusion (1 ug/kg/min), using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays. All of the experiments were conducted with male mice 2.5 months old and included 3 mice per experimental group. Synthesis of cRNA, hybridization and scanning of chips were conducted by Duke University microarray core facility (Duke University, Durham, NC).
2010-09-30 | E-GEOD-18430 | biostudies-arrayexpress
Project description:In order to characterize gene expression networks linked to AT1 angiotensin receptors in the kidney, we carried out genome-wide transcriptional analysis of RNA from kidneys of wild-type (WT) and AT1A receptor-deficient mice (KOs) at baseline and after 2 days of angiotensin II infusion (1 ug/kg/min), using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays. At baseline, 405 genes were differentially expressed (>1.5X) between WT and KO kidneys. Of these, more than 80% were up-regulated in the KO group including genes involved in inflammation, oxidative stress, and cell proliferation. After 2 days of angiotensin II infusion in WT mice, expression of ~805 genes was altered (18% up-regulated, 82% repressed). Genes in metabolism and ion transport pathways were up-regulated while there was attenuated expression of protective genes against oxidative stress including glutathione synthetase and mitochondrial SOD2. Angiotensin II infusion has little effect on blood pressure in KOs. Nonetheless, expression of more than 250 genes was altered in kidneys from KO mice during angiotensin II infusion; 14% were up-regulated, while 86% were repressed including genes involved in immune responses, angiogenesis, and glutathione metabolism. Between WT and KO kidneys during angiotensin II infusion, 728 genes were differentially expressed; 10% were increased and 90% were decreased in the WT group. Differentially regulated pathways included those involved in ion transport, immune responses, metabolism, apoptosis, cell proliferation, and oxidative stress. This genome-wide assessment should facilitate identification of critical distal pathways linked to blood pressure regulation.
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Project description:Angiotensin II (Ang II) mediated signaling plays a key role in the development of hypertension associated target organ damages. However, the gene expression changes regulated by Ang II in the early stage of acute cerebral, cardiac, renal, vascular injury remain unclear. we investigated Ang II–mediated gene expression alteration associated with the development of early cerebral, cardiac, renal, vascular injury by microarray assay in a mouse model.
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Project description:We use next-generation sequencing (NGS) to profile miRNA in small arteries of mice infused with angiotensin (Ang) II for 7 and 14 days. The goal is to identify differentially expressed miRNAs that are associated with Ang II-induced vascular injury and hypertension.
2019-05-22 | GSE101704 | GEO
Project description:To explore the role of endothelial cells in hypertension, we developed an angiotensin II-induced mouse hypertension model. Eight-week-old C57BL/6 mice were anesthetized using 2% pentobarbital sodium, and osmotic pumps were subcutaneously implanted to deliver AngII at a constant rate of 1000 ng/kg/min over 14 consecutive days. Sham-operated mice underwent the identical procedure, with osmotic pumps containing 0.9% saline implanted subcutaneously instead. Subsequently, mouse aortic endothelial cells were isolated and subjected to RNA sequencing analysis.
2026-01-01 | GSE304402 | GEO
Project description:In this study we used microarrays to examine relative genes expression within the aorta of ApoE-/- infused with angiotensin II in relation to aneurysm formation. Infusion of angiotensin II induces aortic dilatation particularly of the suprarenal aorta in ApoE-/- mice. Based on studies carried out in our and other laboratories the response to angiotensin II is variable, with some mice developing large aneurysms but other animals appearing resistant to aneurysm formation with aortic diameters similar to that of saline controls. We compared RNA expression from whole aortas of 17 week old male ApoE-/- mice exposed to angiotensin II (1.44 µg/kg/min) for 4 weeks where there was clear evidence of aortic aneurysm formation (n=5) with that of mice failing to develop aneurysms (n=7) and those exposed to saline infusion (n=6). AAA was defined as diameter of suprarenal aorta greated than 1.5mm measured on photographs of aortas at necroscopy. Keywords: Disease state analysis 18 samples analysed, AAA (n=5), no AAA (n=7), saline (n=6). AAA - abdominal aortic aneurysm
2010-06-24 | E-GEOD-12591 | biostudies-arrayexpress
Project description:We used next-generation sequencing (NGS) to profile total RNA in small arteries of mice infused or not with angiotensin (Ang) II for 7 and 14 days. The goal was to identify differentially expressed genes that are associated with Ang II-induced vascular injury and hypertension.
2019-05-22 | GSE101707 | GEO
Project description:In this study we used microarrays to examine relative genes expression within the aorta of ApoE-/- infused with angiotensin II in relation to aneurysm formation. Infusion of angiotensin II induces aortic dilatation particularly of the suprarenal aorta in ApoE-/- mice. Based on studies carried out in our and other laboratories the response to angiotensin II is variable, with some mice developing large aneurysms but other animals appearing resistant to aneurysm formation with aortic diameters similar to that of saline controls. We compared RNA expression from whole aortas of 17 week old male ApoE-/- mice exposed to angiotensin II (1.44 µg/kg/min) for 4 weeks where there was clear evidence of aortic aneurysm formation (n=5) with that of mice failing to develop aneurysms (n=7) and those exposed to saline infusion (n=6). AAA was defined as diameter of suprarenal aorta greated than 1.5mm measured on photographs of aortas at necroscopy. Keywords: Disease state analysis
2009-08-26 | GSE12591 | GEO