RNA sequencing of healthy and diseased (idiopathic pulmonary hypertension) human pulmonary artery smooth muscle cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA603286 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10969436.fastq.gz | Fastqsanger.gz | |||
| SRR10969437.fastq.gz | Fastqsanger.gz | |||
| SRR10969438.fastq.gz | Fastqsanger.gz | |||
| SRR10969439.fastq.gz | Fastqsanger.gz | |||
| SRR10969440.fastq.gz | Fastqsanger.gz |
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Project description:We performed RNA-seq to analyze gene expression in human PASMCs (Pulmonary arterial smooth muscle cells) isolated from subjects without disease and from subjects with IPAH (idiopathic pulmonary hypertension)
2020-07-15 | GSE144274 | GEO
Project description:Despite recent improvements in management of idiopathic pulmonary arterial hypertension, mortality remains high. Understanding the alterations in the transcriptome–phenotype of the key lung cells involved could provide insight into the drivers of pathogenesis. In this study, we examined differential gene expression of cell types implicated in idiopathic pulmonary arterial hypertension from lung explants of patients with idiopathic pulmonary arterial hypertension compared to control lungs. After tissue digestion, we analyzed all cells from three idiopathic pulmonary arterial hypertension and six control lungs using droplet-based single cell RNA-sequencing. After dimensional reduction by t-stochastic neighbor embedding, we compared the transcriptomes of endothelial cells, pericyte/smooth muscle cells, fibroblasts, and macrophage clusters, examining differential gene expression and pathways implicated by analysis of Gene Ontology Enrichment. We found that endothelial cells and pericyte/smooth muscle cells had the most differentially expressed gene profile compared to other cell types. Top differentially upregulated genes in endothelial cells included novel genes: ROBO4, APCDD1, NDST1, MMRN2, NOTCH4, and DOCK6, as well as previously reported genes: ENG, ORAI2, TFDP1, KDR, AMOTL2, PDGFB, FGFR1, EDN1, and NOTCH1. Several transcription factors were also found to be upregulated in idiopathic pulmonary arterial hypertension endothelial cells including SOX18, STRA13, LYL1, and ELK, which have known roles in regulating endothelial cell phenotype. In particular, SOX18 was implicated through bioinformatics analyses in regulating the idiopathic pulmonary arterial hypertension endothelial cell transcriptome. Furthermore, idiopathic pulmonary arterial hypertension endothelial cells upregulated expression of FAM60A and HDAC7, potentially affecting epigenetic changes in idiopathic pulmonary arterial hypertension endothelial cells. Pericyte/smooth muscle cells expressed genes implicated in regulation of cellular apoptosis and extracellular matrix organization, and several ligands for genes showing increased expression in endothelial cells. In conclusion, our study represents the first detailed look at the transcriptomic landscape across idiopathic pulmonary arterial hypertension lung cells and provides robust insight into alterations that occur in vivo in idiopathic pulmonary arterial hypertension lungs.
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Project description:Pulmonary hypertension (PH) is a common complication of systemic sclerosis (SSc) and a leading cause of mortality among patients with this disease. PH can also occur as an idiopathic condition (idiopathic pulmonary arterial hypertension, iPAH). We sought to investigate the transcriptomic alterations in PH vascular populations to understand cellular mechanisms underlying pathobiology of systemic sclerosis associated and idiopathic pulmonary hypertension.
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Project description:Bone morphogenetic proteins (BMP) inhibit proliferation and induce apoptosis in pulmonary artery smooth muscle cells (PASMC) from normal subjects. Dysfunction of BMP signaling due to mutations in and/or downregulation of BMP receptors has been implicated in idiopathic pulmonary arterial hypertension (IPAH). We examined whether BMP differentially regulates gene expression in PASMC from normal subjects and IPAH patients using the Affymetrix microarray analysis. BMP-2 treatment (200 nM for 24 hrs) altered expression levels of 6,206 genes in normal and IPAH PASMC. 1,063 of these genes were regulated oppositely by BMP-2: 523 genes were downregulated by BMP-2 in normal PASMC but upregulated in IPAH PASMC, whereas 540 genes were upregulated by BMP-2 in normal PASMC but downregulated in IPAH PASMC. The divergent effects of BMP-2 on gene expression profiles indicate that PASMC may undergo significant phenotypic changes in IPAH patients during development of the disease. The transition of the antiproliferative effect of BMP-2 in normal PASMC to its proliferative effect in IPAH patients is attributed potentially to its differential effect on expression patterns of various genes that are involved in cell proliferation and apoptosis. Among the 6206 BMP-2-sensitive genes, there are more than 1800 genes whose expression levels were negatively (with a correlation coefficient, r, < –0.9) or positively (with r > +0.9) correlated with the pulmonary arterial pressure. These results suggest that BMP-mediated gene regulation is significantly altered in PASMC from IPAH patients and mRNA expression changes in BMP-regulated genes may be involved in the development of IPAH. Keywords = bone morphogenetic receptor protein Keywords = idiopathic pulmonary arterial hypertension Keywords = transcription factor Keywords = gene expression profile Keywords: other
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Project description:Transcriptional Profiles of Pulmonary Artery Endothelial Cells in Pulmonary Hypertension
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Project description:RAB7 deficiency impairs pulmonary artery endothelial function and promotes pulmonary hypertension
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Project description:Right heart failure results from advanced pulmonary hypertension (PH) and has a poor prognosis. There are few available treatments for right heart failure. Pulmonary artery remodeling, including changes in pulmonary artery endothelial cells to endothelial-mesenchymal cells, and aberrant fibroblast and pulmonary artery smooth muscle cell (PASMC) proliferation, are characteristics of the pathophysiological process of PH. As a result, the clinical situation requires novel PH diagnostic and treatment targets.
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Project description:Pulmonary arterial hypertension (PAH) is characterized by endothelial cell (EC) dysfunction. There are no data from living patients to inform whether differential gene expression of pulmonary artery ECs (PAECs) can discern disease subtypes, progression and pathogenesis. We aimed to further validate our previously described method to propagate ECs from right heart catheter (RHC) balloon tips and to perform additional PAEC phenotyping. We performed bulk RNA sequencing of PAECs from RHC balloons. Using unsupervised dimensionality reduction and clustering we compared transcriptional signatures from PAH to controls and other forms of pulmonary hypertension. Select PAEC samples underwent single cell and population growth characterization and anoikis quantification. Fifty-four specimens were analyzed from 49 subjects. The transcriptome appeared stable over limited passages. Six genes involved in sex steroid signaling, metabolism, and oncogenesis were significantly upregulated in PAH subjects as compared to controls. Genes regulating BMP and Wnt signaling, oxidative stress and cellular metabolism were differentially expressed in PAH subjects. Changes in gene expression tracked with clinical events in PAH subjects with serial samples over time. Functional assays demonstrated enhanced replication competency and anoikis resistance. Our findings recapitulate fundamental biological processes of PAH and provide new evidence of a cancer-like phenotype in ECs from the central vasculature of PAH patients. This “cell biopsy” approach may provide insight into EC heterogeneity within the lung and a therapeutic screening approach in PAH.
2023-12-27 | GSE243193 | GEO
Project description:Pulmonary hypertension (PH) is a progressive disease with a high mortality rate, usually as a result of right heart failure. The pulmonary vasculature in PH is characterized by remodeling and stiffening, potentially with luminal obstruction, driven by enhanced cell proliferation/survival versus cell death, chronic inflammation, and altered extracellular matrix (ECM), with an increase in vascular fibrosis. Given the poorly understood biochemical nature of pulmonary vascular remodeling, we evaluated the ECM and ECM-associated protein composition of the main pulmonary artery (MPA), distal pulmonary arteries (DPA) distal whole lung (DWL) of acute hypoxia-driven PH (in a young bovine calf model) using high-resolution mass spectrometry. Significant differences in the proteomic signatures were observed in the three vascular/tissue sites. Alterations included a strong immune response and wound repair signature including several proteins from the coagulation cascade and markers of a provisional matrix. These findings support a role for disease propagation that proceeds through a wound-healing trajectory with a strong hemostasis and provision matrix in the MPA, to a more destructive remodeling with higher turnover in the most distal capillaries. This data provides insight into short-term remodeling that results in robust biomechanical manifestation of PH and initiates a resolvable disease trajectory when hypoxic insult is removed.
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Project description:The hypothesis tested in this study was that chronic exposure of PBMCs to a hypertensive environment in remodeled pulmonary vessels would be reflected by specific transcriptional changes in these cells. The transcript profiles of PBMCs from 30 idiopathic pulmonary arterial hypertension patients (IPAH), 19 patients with systemic sclerosis without pulmonary hypertension (SSc), 42 scleroderma-associated PAH patients (SSc-PAH), and 8 patients with SSc complicated by interstitial lung disease and PH (SSC-PH-ILD) were compared to the gene expression profiles of PBMCs from 41 healthy individuals. Gene expression is compared at a global level using total RNA from BPMC for pateints and controls using the Illumina microarray platform.
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