Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomics analysis of the myocardium form chronic hypobaric hypoxia-induced mice model

ABSTRACT: C57BL/6J mice were assigned to the hypobaric hypoxia chamber for simulation of high-altitude conditions. iTRAQ proteomics analysis/nanoUHPLC-MS/MS analysis was performed accordingly in the right myocardium of mice that had been allowed to develop hypoxia-induced pulmonary hypertension after hypobaric hypoxia exposure.

ORGANISM(S): Mus Sp.

SUBMITTER: Jie Yang

PROVIDER: PXD040342 | iProX | Thu Feb 23 00:00:00 GMT 2023

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Mitochondria-associated membrane protein PACS2 maintains right cardiac function in hypobaric hypoxia.

Yang Jie J Sun Mengjia M Chen Renzheng R Ye Xiaowei X Wu Boji B Liu Zhen Z Zhang Jihang J Gao Xubin X Cheng Ran R He Chunyan C He Jingyu J Wang Xuhong X Huang Lan L

iScience 20230305 4

Hypobaric hypoxia (HH) is the primary challenge at highland. Prolonged HH exposure impairs right cardiac function. Mitochondria-associated membrane (MAM) plays a principal role in regulating mitochondrial function under hypoxia, but the mechanism was unclear. In this study, proteomics analysis identified that PACS2, a key protein in MAM, and mitophagy were downregulated in HH. Metabolomics analysis indicated suppression of glucose and fatty acids aerobic oxidation in HH conditions. Cardiomyocyte ...[more]

PMID: 36968068

Similar Datasets

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

Transcription profiling of mouse exposed to chronic hypoxia

Project description:High altitude environments are characterized by the unique and unavoidable stress of chronic hypoxia. While much is known about gene expression responses to acute or in vitro hypoxia, less is known about the gene expression profiles of animals exposed to systemic chronic hypoxia, such as that experienced at high elevations. Here we simulated the hypoxic environment of two high altitude elevations,and a third chamber recieved ambient Reno air. Mice were housed in the hypoxic chambers for 32 days. We used microarrays to characterize the differential gene expression in the livers of mice housed in hypoxic environment of 4500 m versus 3000 and 1400 m. We used this data to draw hypotheses related to novel physiological responses to chronic systemic hypoxia Experiment Overall Design: Mice were housed one of three chambers; the first received ambient Reno air (1400 m) and the other two received air mixed with nitrogen such that one chamber simulated the hypoxic environment of 3000 m and the third chamber simulated hypoxic environment of 4500 m. Twelve mice were housed in each chamber for 32 days. Liver were extracted, and RNA from livers of 4 mice were pooled such that each treatment was represented by 3 pooled samples. Eight of the nine arrays were used for data analysis; one array was excluded as several Affymetrix quality control metrics indicated data quality that was not reliable.

2009-05-11 | E-GEOD-15891 | biostudies-arrayexpress

Gene expression of Mus exposed to chronic hypoxia

2009-04-30 | GSE15891 | GEO

Lung transcriptomes of wild type, β-arrestin 1 -/-, and β-arrestin 2 -/- mice exposed to normoxia or chronic hypoxia

Project description:We found that β-arrestin 1 -/- mice were more sensitive to hypoxia-induced pulmonary arterial hypertension with increased right ventricle hypertrophy and higher right ventricle systolic pressure, while β-arrestin 2 -/- mice developed right ventricle hypertrophy comparable to wild type mice. Moreover, β-arrestin 1 -/- mice had worse right ventricle function than wild type mice in response to chronic hypoxia, whereas β-arrestin 2 -/- mice relatively preserved right ventricle function compared to wild type mice. To investigate the molecular mechanisms responsible for the worse PAH in β-arrestin 1 -/- mice, we performed lung transcriptome analysis of wild type, β-arrestin 1 -/-, and β-arrestin 2 -/- mice using high-throughput RNA-seq.

2018-11-19 | GSE110131 | GEO

Combined intermittent and sustained hypoxia is a novel and deleterious cardio-metabolic phenotype

Project description:Study objectives: Chronic obstructive pulmonary disease and obstructive sleep apnea overlap syndrome is associated with excess mortality, and outcomes are related to the degree of hypoxemia. People at high altitude are susceptible to periodic breathing, and hypoxia at altitude is associated with cardio-metabolic dysfunction. Hypoxemia in these scenarios may be described as superimposed sustained plus intermittent hypoxia, or overlap hypoxia (OH), the effects of which have not been investigated. We aimed to characterize the cardio-metabolic consequences of OH in mice. Methods: C57BL/6J mice were subjected to either sustained hypoxia (SH, FiO2=0.10), intermittent hypoxia (IH, FiO2=0.21 for 12 hours, and FiO2 oscillating between 0.21 and 0.06, 60 times/hour, for 12 hours), OH (FiO2=0.13 for 12 hours, and FiO2 oscillating between 0.13 and 0.06, 60 times/hour, for 12 hours), or room air (RA), n=8/group. Blood pressure and intraperitoneal glucose tolerance test were measured serially, and right ventricular systolic pressure (RVSP) was assessed. Results: Systolic blood pressure transiently increased in IH and OH relative to SH and RA. RVSP did not increase in IH, but increased in SH and OH by 52% (p<0.001) and 20% (p=0.001). Glucose disposal worsened in IH and improved in SH, with no change in OH. Serum LDL and VLDL increased in OH and SH, but not in IH. Hepatic oxidative stress increased in all hypoxic groups, with the highest increase in OH. Conclusions: Overlap hypoxia may represent a unique and deleterious cardio-metabolic stimulus, causing systemic and pulmonary hypertension, and without protective metabolic effects characteristic of sustained hypoxia.

2021-12-01 | GSE189958 | GEO

Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling

Project description:Using a combination of single-cell RNAseq methods and murine pulmonary hypertension models, we show HIF2α overexpressing pericytes’ transformation into SMC-like cells, confirming HIF2α as a major molecular regulator in hypoxia-induced pulmonary hypertension (PH) and vascular remodeling. We demonstrate that HIF2α overexpression in pericyte-dominant transgenic mice exacerbates PH and right ventricular hypertrophy (RVH), whereas disruption of HIF2α expression attenuates the development of PH.

2024-08-25 | GSE211985 | GEO

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.

2021-03-04 | GSE168159 | GEO

Hypoxia-induced pulmonary hypertension in calf right ventricle

Project description:Hypoxia-induced pulmonary hypertension in calf right ventricle

| PRJNA899456 | ENA

Parathyroid hormone exacerbates pulmonary hypertension through hypoxia-induced parathyroid hormone receptor upregulation.

Project description:Pulmonary hypertension (PH) is an incurable right heart failure disease. Parathyroid hormone (PTH) is secreted from the parathyroid gland and plays a crucial role in calcium homeostasis. PTH also acts on the cardiovascular system and affects cardiovascular prognosis. We assessed whether the regulation of PTH affected PH in a hypoxia (Hx)-induced PH mouse model. PTH treatment exacerbated right ventricular hypertrophy and right ventricular systolic pressure in Hx mice. Our data showed how is PTH effected for PH model murine lung.

2023-10-11 | GSE244861 | GEO

MiR-19b-1 drives gestational hypoxia-Induced pulmonary hypertension through NADPH oxidases

Project description:Gestational hypoxia can lead to intrauterine growth restriction and programming of cardiovascular diseases in adulthood via different, although not completely understood, epigenetic mechanisms. Reactive oxygen species (ROS) have been suggested to contribute to fetal programming, although their source and specific role is not well understood. We have previously shown that reactive oxygen species (ROS) derived from NADPH oxidases contribute to hypoxia induced pulmonary hypertension. However, their role in disease programming by gestational hypoxia is not resolved. We aimed to elucidate the role of NADPH oxidases and redox sensitive miRNAs in the cardiovascular response of adult offspring to transient gestational hypoxia. In this study, we demonstrate that gestational hypoxia programs pulmonary hypertension in adulthood by upregulating NADPH oxidases and downregulating miR-19b-1 subsequently affecting the mTOR pathway. Since dysregulation of miR-19b-1 induced not only pulmonary hypertension but was also associated with right ventricular pressure in congenital heart defects patients, these findings might open novel options for diagnosis, prevention and treatment of right heart disease.

2025-09-17 | GSE243467 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data