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A Validated Gene Signature from Peripheral Blood Mononuclear Cells in Pulmonary Hypertension Associated with Sickle Cell Disease

ABSTRACT: Pulmonary hypertension (PH) is a serious complication of sickle cell disease (SCD) associated with increased mortality. Gene expression profiles of peripheral blood mononuclear cells (PBMC) have been studied in pulmonary arterial hypertension and in SCD. We hypothesized that a PBMC-derived gene signature in SCD patients may be utilized as a PH biomarker. Twenty-seven patients with homozygous SCD underwent transthoracic echocardiography and PBMC isolation. PH was defined as estimated right ventricular systolic pressure (RVSP)>30 mmHg with a peak tricuspid regurgitation velocity (TRV)>2.5m/s. Genome-wide gene expression profiles were correlated against PH severity using RVSP and TRV as surrogates, which yielded 631 potentially dysregulated transcripts.

ORGANISM(S): Homo sapiens

PROVIDER: GSE38528 | GEO | 2012/06/07

SECONDARY ACCESSION(S): PRJNA168166

REPOSITORIES: GEO

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A Validated Gene Signature from Peripheral Blood Mononuclear Cells in Pulmonary Hypertension Associated with Sickle Cell Disease

Project description:Pulmonary hypertension (PH) is a serious complication of sickle cell disease (SCD) associated with increased mortality. Gene expression profiles of peripheral blood mononuclear cells (PBMC) have been studied in pulmonary arterial hypertension and in SCD. We hypothesized that a PBMC-derived gene signature in SCD patients may be utilized as a PH biomarker. Twenty-seven patients with homozygous SCD underwent transthoracic echocardiography and PBMC isolation. PH was defined as estimated right ventricular systolic pressure (RVSP)>30 mmHg with a peak tricuspid regurgitation velocity (TRV)>2.5m/s. Genome-wide gene expression profiles were correlated against PH severity using RVSP and TRV as surrogates, which yielded 631 potentially dysregulated transcripts. Total RNA was isolated from PBMCs using standard molecular biology protocols without DNA contamination or RNA degradation. Sample processing (e.g., cDNA generation, fragmentation, end labeling, hybridization to Affymetrix GeneChip Human Exon 1.0 ST arrays) was performed per manufacturer’s instructions. A total of 27 African descent American patients with sickle cell disease were included in the microarray analysis.

2012-06-06 | E-GEOD-38528 | biostudies-arrayexpress

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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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Fatty acid-binding proteins contribute to the pathogenesis of pulmonary hypertension [bulk RNA-seq]

Project description:Rationale: Pulmonary arterial hypertension (PAH) is a devastating disease characterized by obliterative vascular remodeling and persistent increase of vascular resistance, leading to right heart failure and premature death. Understanding the cellular and molecular mechanisms will help develop novel therapeutic approaches for PAH patients. Objectives: To determine whether upregulation of fatty-acid binding protein 4 and 5 (FABP4/5) is critical in pathogenesis of PAH. Methods: FABP4/5 expression was examined in pulmonary arterial endothelial cells (PAECs) and lung tissues from patients with idiopathic PAH and pulmonary hypertension (PH) rat models. Plasma proteome analysis was performed in human PAH samples. Echocardiography, hemodynamics, histology, and immunostaining were performed to evaluate the lung and heart PH phenotypes in Egln1Tie2Cre (CKO) mice and Egln1Tie2Cre/Fabp4-5-/- (TKO) mice. Measurement and Main Results: Both FABP4 and FABP5 were highly induced in ECs of CKO mice and PAECs from IPAH patients, and in whole lungs of PH rats. Plasma levels of FABP4/5 were upregulated in IPAH patients and directly correlated with severity of hemodynamics and biochemical parameters. Genetic deletion of both Fabp4 and 5 in CKO mice caused a reduction of right ventricular systolic pressure (RVSP) and RV hypertrophy, attenuated pulmonary vascular remodeling and prevented the right heart failure. Fabp4/5 deletion also normalized EC glycolysis, reduced ROS and HIF-2a expression, and decreased aberrant EC proliferation in CKO lungs. Conclusions: PH causes aberrant expression of FABP4/5 in pulmonary ECs which leads to enhanced EC glycolysis and hyperproliferation, contributing to the accumulation of arterial ECs and vascular remodeling and exacerbating the disease.

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