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Hypoxic pulmonary hypertension study

ABSTRACT: These microarray studies were performed using whole lungs of BALB/C mice during development of hypoxia-induced pulmonary hypertension (days 1-21) and resolution of pulmonary hypertension after return to normoxia (days 22-35) . Mice were sampled during nine time-points and each time-point was replicated 4 times (with dye swapping). Keywords = hypoxia Keywords = pulmonary hypertension Keywords: other

ORGANISM(S): Mus musculus

PROVIDER: GSE1909 | GEO | 2005/03/16

SECONDARY ACCESSION(S): PRJNA90925

REPOSITORIES: GEO

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Hypoxic pulmonary hypertension study

Project description:These microarray studies were performed using whole lungs of BALB/C mice during development of hypoxia-induced pulmonary hypertension (days 1-21) and resolution of pulmonary hypertension after return to normoxia (days 22-35) . Mice were sampled during nine time-points and each time-point was replicated 4 times (with dye swapping). Keywords = hypoxia Keywords = pulmonary hypertension

2010-06-10 | E-GEOD-1909 | biostudies-arrayexpress

LncRNAs and mRNAs profile suggested CCL / CXCL were involved in the reoxygenation reversal of hypoxic pulmonary hypertension in mice

Project description:The potential roles of mRNAs and lncRNAs in the development and the reoxygenation treatment of reversal of hypoxic pulmonary hypertension are still unknown. 24 healthy adult male C57/BL6 mice were divided into three groups (normoxia group, hypoxia group, hypoxia-normoxia group), lncRNA and mRNA microarray was performed，meanwhile，the changes of right ven-tricular systolic pressure (RVSP) and other physiological indexes were measured in the three groups. The results showed that the index of RVSP, the right ventricular hypertrophy index RV/(LV+S), pulmonary artery walls and the muscularization ratio of pulmonary arterioles were significantly increased after Hypoxia treatment, while they were attenuated after the normoxia condition restored. Moreover, the study revealed there were 62 lncRNAs and 99 mRNAs with significant difference expression were associated with the reversal of hypoxic pulmonary hypertension by reoxygenation in mice. Furthermore, the pathway enrichment and gene ontology analysis of 99 DEGS were performed. Interestingly, the result suggested that chemokine subfamily CCL2/ CXCL played a role in the occurrence, development and reversion of pulmonary hypertension by reoxygenation. This study was the first time to demonstrate the transcriptome profiles of lncRNAs and mRNAs in the lung tissue during the reversal of hypoxic pulmonary hypertension in mice by reoxygenation, which might further broaden the understanding of the pathogenesis and the therapeutic effect of oxygen recovery of hypoxic pulmonary hypertension.

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The effects of Arginase 2 (Arg2) knockout on chronic hypoxia-induced pulmonary hypertension

Project description:Increased arginase 2 protein expression is associated with endothelial dysfunction and pulmonary hypertension, likely by impairing NO production secondary to substrate availability. Hypoxia induces arginase 2 protein expression contributing to pulmonary vascular cell proliferation. Non-specific arginase inhibitors have been shown to prevent experimental pulmonary hypertension in animal models. RNA was isolated from whole lung tissue from adult (12-14 weeks) arginase 2 wild type and KO mice exposed to 21% O2 or 10% O2 for 28 days. Animals were sacrificed and the lungs collected and stored at -80°C . Total RNA was isolated with Trizol and used for RNA-seq. RNA-seq results indicate notable differentially expressed gene transcripts were evident in the Arg2 WT and Arg2 KO lungs. There were 25 unique transcripts identified (>2-fold change, p < 0.001) between the normoxia and hypoxia-exposed Arg2 WT. Interestingly, there was significantly greater differences in the Arg2 KO mice exposed to hypoxia compared to normoxia, with 188 unique transcripts (>2-fold change, p < 0.001) identified by RNA seq.

2020-05-01 | GSE131425 | GEO

Analysis of lung transcriptome of Mice under normoxia or hypoxia conditions and treated with ABT-263 or its vehicle during 2 days

Project description:To explore the role played by senescent cells in mice models of pulmonary hypertension we exposed young C57BL6/j mice to 2 days hypoxia or normoxia and treated with senolytic drug ABT-263 (50mg/kg/day) or its vehicule. We then performed lung gene expression profiling analysis using data obtained from RNA-seq of 4 groups of mice (Normoxia+Vehicule; Normoxia+ABT-263; Hypoxia+Vehicule; Hypoxia+ABT-263)

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Analysis of lung transcriptome of Mice under normoxia or hypoxia conditions and treated with ABT-263 or its vehicle during 8 days

Project description:To explore the role played by senescent cells in mice models of pulmonary hypertension we exposed young C57BL6/j mice to 8 days hypoxia or normoxia and treated with senolytic drug ABT-263 (50mg/kg/day) or its vehicule. We then performed lung gene expression profiling analysis using data obtained from RNA-seq of 4 groups of mice (Normoxia+Vehicule; Normoxia+ABT-263; Hypoxia+Vehicule; Hypoxia+ABT-263)

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Transcription profiling of normoxic and hypoxic mice to elucidate the genes involved in vascular remodeling following pulmonary hypertension

Project description:Hypoxia can induce vasoconstriction followed by vascular remodeling including hypertrophy and hyperplasia of pulmonary vascular smooth muscle and proliferation of endothelial cells. The goal of this project is to elucidate the genes involved in vascular remodeling following pulmonary hypertension. Total RNA was isolated from lungs of normoxic and hypoxic treated animals.

2007-12-13 | E-GEOD-482 | biostudies-arrayexpress

Vascular remodeling following pulmonary hypertension

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Activation of Lung Macrophages in Hypoxic Pulmonary Hypertension

Project description:Studies in various animal models suggest an important role for pulmonary macrophages in the pathogenesis of pulmonary hypertension (PH). Yet, the molecular mechanisms characterizing the functional macrophage phenotype relative to time and pulmonary localization/compartmentalization remain largely unknown. Here, we utilized a hypoxic murine model of PH in combination with flow cytometry assisted cell sorting (FACS) to quantify and isolate lung macrophages from two compartments over time and characterized their programing via RNA sequencing (RNAseq) approaches. In response to hypoxia, we found an early increase in macrophage number that was restricted to the interstitial/perivascular compartment, without recruitment of macrophages to the alveolar compartment or changes in the number of resident alveolar macrophages. Principle component analysis demonstrated significant differences in overall gene expression between alveolar (AMs) and interstitial macrophages (IMs) at baseline and after 4 and 14 days hypoxic exposure. AM’s at both day 4 and 14 and IM’s at day 4 shared a conserved “hypoxia program” characterized by mitochondrial dysfunction, pro-inflammatory gene activation and mTORC1 signaling, while IM’s at day 14 demonstrated a unique anti-inflammatory/ pro-reparative programming state. We conclude that the pathogenesis of vascular remodeling in hypoxic PH involves an early compartment independent activation of lung macrophages towards a conserved hypoxia program, with the development of compartment specific programs later on in the course of disease. Thus, harnessing time and compartment specific differences in lung macrophage polarization needs to be considered in the therapeutic targeting of macrophages in hypoxic PH and potentially other inflammatory lung diseases.

2017-04-03 | GSE87602 | GEO

Blood pulmonary arterial hypertension

Project description:Microarray analysis of peripheral blood mononuclear (PBMC) cells in pulmonary arterial hypertension. Keywords = mononuclear cells Keywords = gene microarray Keywords = pulmonary arterial hypertension Keywords = Herpesvirus Keywords = biomarker Keywords: other

2003-11-15 | GSE703 | GEO

Intermittent short-duration reoxygenation protects against simulated high altitude-induced pulmonary hypertension in rats

Project description:High-altitude pulmonary hypertension (HAPH) is a severe and progressive disease caused by chronic hypoxia and subsequent pulmonary vascular remodeling. No cure is currently available owing to an incomplete understanding about vascular remodeling. It is believed that hypoxia-induced diseases can be prevented by treating hypoxia. Thus, this study aimed to determine whether daily short-duration reoxygenation at sea level attenuates pulmonary hypertension under high-altitude hypoxia. To this end, a simulated 5,000-m hypoxia rat model was used to evaluate the effect of short-duration reoxygenation. Results show that intermittent, not continuous, short-duration reoxygenation effectively attenuates hypoxia-induced pulmonary hypertension. The mechanisms underlining the protective effects involved that intermittent, short-duration reoxygenation prevented functional and structural remodeling of pulmonary arteries and proliferation, migration, and phenotypic conversion of pulmonary artery smooth muscle cells under hypoxia. The specific genes or potential molecular pathways responsible for mediating the protective effects were also characterised by RNA sequencing.This study is novel in revealing a new potential method in preventing high-altitude pulmonary hypertension. It gives insights into the selection and optimisation of oxygen supply schemes in high-altitude areas.

2020-11-06 | GSE160926 | GEO

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