Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA89945 | ENA |
REPOSITORIES: ENA
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Project description:Renin-angiotensin system (RAS) inhibition reduces stroke and improves brain capillary integrity in stroke prone spontaneously hypertensive rats (SHRSP). We tested the hypothesis that treatment with an angiotensin II receptor subtype 1 (AT1R) antagonist has different effects, compared to an angiotensin converting enzyme (ACE) inhibitor, on gene expression in blood-brain barrier (BBB) capillaries. Six weeks old SHRSP were treated with either olmesartan (4 mg/kg, n=20), lisinopril (6 mg/kg , n=20) or remained untreated (n=20). Blood pressure was controlled by tail-cuff measurement. After 5 weeks the animals were sacrificed and cerebral capillaries were isolated. mRNA was extracted and analyzed with rat GeneChip DNA arrays. Additionally, brain histology and monocyte/macrophage infiltrates were determined. Both treatments similarly reduced neurological signs of stroke, stroke mortality, and monocyte/macrophage infiltration, compared to controls. Blood pressure was not influenced significantly by both drugs. We found 42 transcripts that were regulated by both treatments in the same manner. These genes were mostly related to inflammation. We also observed 39 differentially expressed genes between the two treatment groups that typically contribute to cell growth and differentiation. This study demonstrates that, despite similar effects on cerebral pathology and outcome, ACE inhibition and AT1R blockade have distinct molecular effects on gene expression in BBB capillaries. Keywords = angiotensin II Keywords = gene expression Keywords = microarrays Keywords = brain capillaries Keywords = SHRSP Keywords = olmesartan Keywords = lisinopril Keywords: other
2004-08-31 | GSE1548 | GEO
Project description:Renin-angiotensin system (RAS) inhibition reduces stroke and improves brain capillary integrity in stroke prone spontaneously hypertensive rats (SHRSP). We tested the hypothesis that treatment with an angiotensin II receptor subtype 1 (AT1R) antagonist has different effects, compared to an angiotensin converting enzyme (ACE) inhibitor, on gene expression in blood-brain barrier (BBB) capillaries. Six weeks old SHRSP were treated with either olmesartan (4 mg/kg, n=20), lisinopril (6 mg/kg , n=20) or remained untreated (n=20). Blood pressure was controlled by tail-cuff measurement. After 5 weeks the animals were sacrificed and cerebral capillaries were isolated. mRNA was extracted and analyzed with rat GeneChip DNA arrays. Additionally, brain histology and monocyte/macrophage infiltrates were determined. Both treatments similarly reduced neurological signs of stroke, stroke mortality, and monocyte/macrophage infiltration, compared to controls. Blood pressure was not influenced significantly by both drugs. We found 42 transcripts that were regulated by both treatments in the same manner. These genes were mostly related to inflammation. We also observed 39 differentially expressed genes between the two treatment groups that typically contribute to cell growth and differentiation. This study demonstrates that, despite similar effects on cerebral pathology and outcome, ACE inhibition and AT1R blockade have distinct molecular effects on gene expression in BBB capillaries.
2007-10-31 | E-GEOD-1548 | biostudies-arrayexpress
Project description:Expression data from Angiotensin II (Ang II)-treated Rat Vascular Smooth Muscle Cells (RVSMC)
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Project description:Gene expression profiling of aortic media after long-term treatment with an angiotensin II-receptor blocker, Losartan
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Project description:Effect of erythropoietin on cerebral ischemia-induced changes in gene expression in rats
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Project description:The effect of XUESAITONG on gene expression profile after focal cerebral ischemia in rats
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Project description:Knee osteoarthritis (KOA), as a degenerative multifactorial disease, affects the quality of life and mental health of patients, and also brings a huge socioeconomic burden. Treating synovitis have shown promise as anti-inflammatory therapeutics in mitigating OA symptoms and disease progression. Here, by analysing synovial single-cell sequencing (scRNA-seq) data from KOA, we found that synovial fibroblasts (FLS) in OA synovium showed a distinct pro-inflammatory phenotype. We collected synovial tissue from patients with clinical OA as well as from healthy donors, and histological examination was consistent with findings in scRNA-seq. Inspired by recent cross-tissue fibroblast lineage studies, we identified by sequencing that healthy FLS in synovial tissues share transcriptome-level similarities with dermal fibroblasts (DFb). Subsequently, we revealed the local as well as systemic distribution of intra-articular injected DFbs by constructing/extracting two types of rat fibroblasts (luciferase DFbs as well as GFP DFbs). The results demonstrate that DFbs can be locally retained in the synovium for up to three weeks following targeted engrafting on it. And intra-articular injection does not result in DFbs migration to vital organs or the occurrence of histological changes in these organs. A rat model of KOA was constructed by anterior cruciate ligament transection (ACLT) in order to study the therapeutic effect of DFbs on KOA. After injection, the rats showed improvement in painful gait. In addition, histological as well as imaging results showed reduced synovitis and improvement in articular cartilage. Finally we verified the protective effect of DFbs on cytokine-stimulated chondrocytes in a co-culture system.
2026-06-24 | GSE304724 | GEO
Project description:Novel long non-coding RNAs are involved in cellular response to angiotensin II signaling
| PRJNA167134 | ENA
Project description:Inflammation is a key component of pathological angiogenesis. Here we induce cornea neovascularisation using sutures placed into the cornea, and sutures are removed to induce a regression phase. We used whole transcriptome microarray to monitor gene expression profies of several genes
2016-08-18 | GSE81418 | GEO
Project description:Regulation of Angiotensin II Actions by Enhancers and Super-enhancers in Vascular Smooth Muscle Cells
| PRJNA375926 | ENA