Ontology highlight
ABSTRACT:
PROVIDER: PRJNA941949 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23719556_1.fastq.gz | Fastqsanger.gz | |||
| SRR23719556_2.fastq.gz | Fastqsanger.gz | |||
| SRR23719557_1.fastq.gz | Fastqsanger.gz | |||
| SRR23719557_2.fastq.gz | Fastqsanger.gz | |||
| SRR23719558_1.fastq.gz | Fastqsanger.gz |
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Project description:Long-term arterial hypertension causes cerebral microvascular dysfunction and doubles dementia risk in aging. However, cognitive health preservation by therapeutical blood pressure lowering alone might be limited by disease duration, the degree of irreversible tissue damage and whether microvascular function can be restored. This study aimed to understand cellular and molecular temporo-spatial pathomechanisms in the course of arterial hypertension. We investigated initial, early chronic and late chronic hypertension effects in the frontal brain of hypertensive rats by applying behavioral tests, histology, immunofluorescence, FACS and microvascular/neural tissue RNA sequencing as well as 18F-FDG PET imaging. Chronic hypertension caused frontal brain-specific behavioral deficits. From a mechanistic perspective our results suggest continuous microvascular stress and wounding due to hypertension, which in turn leads to an early recruitment of activated microglia and peripheral immune cells, blood-brain-barrier breakdown and an energy-demanding hypermetabolic state. Vascular adaptation mechanisms e.g., vessel wall strengthening by production of cellular adhesion molecules and extracellular matrix (ECM), and angiogenesis were first observed first in late chronic stages. Additionally, we identified late-chronic vascular accumulation of Igfbp-5 in the brains of rats and humans with hypertensive cerebral small vessel disease, possibly attenuating protective Igf-1 signaling in the cerebral microvasculature. Thus, we characterized cellular and molecular temporo-spatial pathomechanisms in the course of arterial hypertension, that might represent critical points for clinical decision-making and could therefore be used to prevent irreversible tissue damage.
2026-01-01 | GSE223851 | GEO
Project description:Using data-independent acquisition-based mass spectrometry analysis, we determined the protein changes in cerebral arteries in pre- and early-onset hypertension from the spontaneously hypertensive rat (SHR), a model that resembles essential hypertension. Our analysis identified 125 proteins with expression levels that were significantly up- or downregulated in 12-week old SHRs compared to normotensive Wistar Kyoto rats. Using an angiogenesis enrichment analysis, we identified a critical imbalance in angiogenic proteins, promoting an anti-angiogenic profile in cerebral arteries at the early-onset of hypertension. In a comparison to previously published data, we demonstrate that this angiogenic imbalance is not present in mesenteric and renal arteries from age-matched SHRs. Finally, we identified two proteins (Fbln5 and Cdh13), whose expression levels were critically altered in cerebral arteries compared to the other arterial beds. The observation of an angiogenic imbalance in cerebral arteries from the SHR reveals critical protein changes in the cerebrovasculature at the early-onset of hypertension and provides novel insight into the early pathology of cerebrovascular disease.
2023-09-20 | PXD040818 | Pride
Project description:<p>Background: Hypertension remains a significant global health challenge, with limited treatment efficacy in many patients. Emerging evidence suggests that gut microbiota plays a crucial role in blood pressure regulation. This study investigates the anti-hypertensive effects of Achyranthes bidentata (Ab) extract and its interaction with the gut microbiota, particularly focusing on the enrichment of Dubosiella sp. and its impact on arachidonic acid metabolism.</p><p>Results: Here, we identified a novel microbiota-driven anti-hypertensive mechanism mediated by the Ab extract and Dubosiella sp. Ab significantly ameliorated hypertension and kidney damage by enriching Dubosiella in hypertensive mice. Metabolomics analysis revealed that Ab enhances lipid metabolic pathways, particularly arachidonic acid metabolism. In vitro, Ab significantly promoted the biofilm formation of D. newyorkensis DSM103457. Further gavage experiments confirmed that D. newyorkensis DSM103457 alleviates hypertension, cardiac and kidney injury. Combined microbial and metabolic profiling via 16S rRNA sequencing, metagenomics and metabolomics demonstrated that D. newyorkensis DSM103457 modulates gut microbiota, arachidonic acid metabolism, restoring prostaglandins and leukotrienes essential for cardiovascular homeostasis. Notably, arachidonic acid significantly promotes D. newyorkensis DSM103457 growth, enabling rapid generation and transformation of HETEs and HODEs in vitro.</p><p>Conclusions: This study identified Ab-Dubosiella-arachidonic acid axis as a novel anti-hypertensive pathway, offering promise for the development of integrated herbal prebiotics and microbial probiotics for targeted hypertension therapy.</p>
2025-04-02 | MTBLS11993 | MetaboLights
Project description:<p>We identify a novel microbiota-driven anti-hypertensive mechanism mediated by Achyranthes bidentata (Ab) extract and gut microbe Dubosiella sp.. Using a hypertensive mouse model induced by L-NAME and a high-salt diet, we show that Ab extract significantly ameliorates hypertension and renal damage by selectively enriching Dubosiella in the gut microbiota. Metabolomics suggested that Ab significantly changed the metabolic profiles and enriched the lipid metabolism including arachidonic acid metabolism. In vitro, Ab significantly promote the biofilm formation of Dubosiella DSM103457. Further gavage experiments with Dubosiella DSM103457 confirmed its effects of alleviating hypertension and heart injury. Microbial and metabolic profiling via 16S rRNA sequencing, metagenomics and metabolomics revealed that Dubosiella DSM103457 modulates arachidonic acid metabolism, restoring critical prostaglandins and leukotrienes associated with cardiovascular homeostasis.</p>
2025-04-02 | MTBLS12017 | MetaboLights
Project description:The composition of cardiac EVs (cEVs) isolated from hypertensive mice and their capacity to reprogram cardiac fibroblasts was investigated using mass spectrometry-based proteomic profiling. Hypertensive and recovering cEVs displayed altered presence of proteins involved in peptidase activity, response to oxygen radical, and glycerolipid metabolism. Following their uptake to cardiac fibroblasts, cEV treatment from normotensive animals resulted in potent antifibrotic and prohomeostatic functions, with sex dependent differences in RNA splicing and energy metabolism proteins.Bioinformatic analysis of hypertensive-cEV remodelled fibroblasts revealed disease associated profibrotic signalling, and sex specific influences on components involved in antioxidant activity, RNA metabolism, fatty acid metabolism, and glycosylation processing. Moreover, investigation of temporal cEV signalling across hypertension and recovery revealed dynamic sex and disease dependent reprogramming of proteins related to RNA binding, interferon signalling, protein glycosylation, ECM regulation, signal transduction, and protein and energy metabolisms. We highlight the dynamic composition and signalling of cEVs in regulating fibroblast biology, reporting sex-dependent differences in cardiac physiology and hypertension.
2023-06-27 | MSV000092292 | MassIVE
Project description:We aimed to investigate the microbial community composition in patients with intracerebral hemorrhage (ICH) and its effect on prognosis. The relationship between changes in bacterial flora and the prognosis of spontaneous cerebral hemorrhage was studied in two cohort studies. Fecal samples from healthy volunteers and patients with intracerebral hemorrhage were subjected to 16S rRNA sequencing at three time points: T1 (within 24 hours of admission), T2 (3 days post-surgery), and T3 (7 days post-surgery) using Illumina high-throughput sequencing technology.
2024-08-22 | E-MTAB-14351 | biostudies-arrayexpress
Project description:We hypothesize blood breakdown products present after hemorrhage to be inducers of brain edema via the ferroptosis-induced cell death of pericytes leading to comprimised blood-brain-barrier. RNAseq was applied to investigate the intracellular response of pericytes to iron exposure from cerebral hemorrhage.
2025-03-05 | GSE230184 | GEO
Project description:Hypertension is a major risk factor for both stroke and cognitive impairment, but it is unclear whether it may specifically affect post-stroke cognitive impairment. We assessed the effect of hypertension and/or stroke on brain injury, cognitive outcome, and the brain transcriptomic profile. C57BL/6J mice (n=117; 3-5 mo.) received s.c. infusion of either saline or angiotensin II (for 14 d or 28 d) followed by sham surgery or photothrombotic stroke targeting the prefrontal cortex seven days later. Cognitive function was assessed with the Barnes maze. RNA sequencing was used to quantify transcriptomic changes in the brain. Angiotensin II treatment produced spontaneous hemorrhaging on the stroke brain. In the Barnes maze, hypertensive mice that received stroke surgery had an increased escape latency compared to other groups (day 3: hypertensive + stroke=166.6±6.0 s vs. hypertensive + sham=122.8±13.8 s vs. normotensive + stroke=139.9±10.1 s vs. normotensive + sham=101.9±16.7 s), consistent with a greater learning impairment. RNA sequencing revealed >800 differentially expressed genes related to neuroinflammation in hypertensive + stroke vs. hypertensive + sham, which included genes associated with apoptosis, microRNAs, autophagy, anti-cognitive biomarkers and Wnt signaling. The combination of hypertension and stroke resulted in greater learning impairment and brain injury.
2024-11-27 | GSE247789 | GEO
Project description:The role and miRNA expression profile of exosomes in hypertension remain largely unknown, therefore, next generation sequencing was used to define the miRNA expression profile of plasma exosomes in spontaneously hypertensive rats (SHRs), the most widely used animal model of human essential hypertension, and their controls, normotensive Wistar-Kyoto rats (WKYs). Results revealed that percentages of miRNA in the total small RNA isolated from WKYs and SHRs were not significantly different. Twenty-seven miRNAs were significantly differentially expressed (DE) between WKY and SHR exosomes, among which 23 were upregulated and 4 were downregulated in SHR exosomes compared with WKY exosomes. Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis of top 10 DE miRNAs identified hypertension-specific target genes/signaling pathways. In conclusion, our findings indicate the selective packing of miRNA cargoes into exosomes under hypertensive status, while facilitating the development of potential targets for the diagnosis, prevention and treatment of hypertension.
2020-10-30 | GSE106333 | GEO
Project description:Aims: Hypertension poses a significant challenge to vasculature homeostasis and stands as the most common cardiovascular disease in the world. Its effects are especially profound on vasculature-lining endothelial cells that are directly exposed to the effects of excess pressure. Here, we characterize the in vivo transcriptomic response of cardiac endothelial cells to hypertension using the spontaneous hypertension mouse model BPH/2J. Methods and results: Verification of defective endothelial function in the BPH/2J hypertensive mouse strain was followed by acute isolation of cardiac endothelial cells and transcriptional profiling using RNA sequencing. Gene profiles from normotensive BPN/3J mice were compared to hypertensive animals. We observed over 3000 transcriptional differences between groups including pathways consistent with the cardiac fibrosis found in hypertensive animals. Importantly, many of the fibrosis-linked genes also differ between juvenile pre-hypertensive and adult hypertensive BPH/2J mice, suggesting that these transcriptional differences are hypertension-related. We also show that blood pressure normalization with amlodipine resulted in a subset of genes reversing their expression pattern, supporting the hypertension-dependency of altered gene expression. Yet, other transcripts were recalcitrant to therapeutic intervention illuminating the possibility that hypertension may irreversibly alter some endothelial transcriptional patterns. Conclusions: Hypertension has a profound effect on both function and transcription of endothelial cells, the latter of which was only partially restored with normalization of blood pressure. This study represents one of the first to quantify how endothelial cells are reprogrammed at the molecular level in cardiovascular pathology and advances our understanding of the transcriptional events associated with endothelial dysfunction.
2018-04-09 | GSE104530 | GEO