Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA294143 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the results of RNA sequencing of total RNA isolated from human pulmonary microvascular endothelial cells after transfection with human miR-887-3p or a negative control siRNA, both in triplicate.
2020-07-15 | GSE146063 | GEO
Project description:In this study, we analzyed differences in the effect of hypoxia on the transcriptomic profile of cultured human pulmonary artery endothelial cells (HPAECs) vs. human brain microvascular endothelial cells (HBMVECs). To determine which hypoxia-regulated genes were dependent on hypoxia inducible factor 1-alpha (HIF-1alpha), some cells were transfected with an siRNA against HIF-1alpha prior to treatment with hypoxia. At the completion of the treatment protocol, mRNA was isolated using standard methodology and analyzed further by RNA-seq.
2021-01-26 | GSE163827 | GEO
Project description:human pulmonary artery (endothelial and smoorh muscle) cells : control vs ARSB-siRNA transfected
| PRJNA474432 | ENA
Project description:Transcriptional profiling of HPMECs comparing Control siRNA treated with HSP27 siRNA Two-condition experiment, control siRNA vs HSP27 siRNA ; 3 controlsiRNA transfected replicates , 3HSP27 siRNA replicates. Replicates were pooled and hybridized to a single array.
2015-08-29 | E-GEOD-72485 | biostudies-arrayexpress
Project description:MCF7 Cells: Control siRNA -E2 vs. Control siRNA +E2, Control siRNA -E2 vs. PES1 siRNA -E2,Control siRNA -E2 vs. PES1 siRNA +E2
| PRJNA168250 | ENA
Project description:IFNb-1a-induced gene expression analysis in human pulmonary microvascular endothelial cells
| PRJDB10488 | ENA
Project description:Human herpesvirus-8 (HHV-8) is the causative agent of Kaposiâs sarcoma and is associated with the angioproliferative disorders primary effusion lymphoma (PEL) and multicentric Castlemanâs disease (MCD). We have previously described evidence of HHV-8 infection within the pulmonary vasculature of patients with idiopathic pulmonary arterial hypertension (IPAH). We speculated that viral infection of the pulmonary microvascular endothelial cells could cause the angioproliferative phenotype characteristic of severe pulmonary arterial hypertension (PAH). We now demonstrate the ability of HHV-8 to infect human pulmonary microvascular endothelial cells (HPMVECs) in vitro, confirming both latent and lytic infection. HHV-8 infection of HPMVECs resulted in significant changes of gene expression including alterations of pathways integral to both cellular apoptosis and angiogenesis. This infection also results in alterations of genes integral to the bone morphogenic protein (BMP) pathway, including down regulation of bone morphogenic protein receptor 1a (BMPR1a) and bone morphogenic protein 4 (BMP4). Other genes previously implicated in the development of PAH are also altered in expression by HHV-8 infection. These include increased expression of Interleukin-6 (IL-6) and the matrix metalloproteinases (MMP)-1, MMP-2 and MMP-10. Lastly, cells infected with HHV-8 apoptosis resistant. Infection of pulmonary microvascular endothelial cells with human herepesvirus-8 results in alteration of the BMP pathway as well as an anti-apoptotic phenotype, consistent with the development of plexiform lesions characteristic of pulmonary arterial hypertension. Experiment Overall Design: ⢠Direct comparison of HHV8-infected and mock-infected human pulmonary microvascular endothelial cells. Experiment Overall Design: ⢠Triplicate infection and mock infection samples were prepared. One hybridization per sample, 6 total hybridizations Experiment Overall Design: ⢠Single channel hybridization (no reference).
2008-06-14 | E-GEOD-6489 | biostudies-arrayexpress
Project description:Total RNA was isolated from human pulmonary microvascular endothelial cells (HPMVEC) overexpressed with GFP or TMEM100
2022-10-08 | GSE209868 | GEO
Project description:Physiological shear stress, produced by blood flow, homeostatically regulates the phenotype of pulmonary endothelial cells exerting anti-inflammatory and anti-thrombotic actions and maintaining normal barrier function. In the pulmonary circulation hypoxia, due to high altitude or diseases such as COPD, causes vasoconstriction, increased vascular resistance and pulmonary hypertension. Hypoxia-induced changes in endothelial function play a central role in the development of this pulmonary hypertension. However, the direct interactive effects of hypoxia and shear stress on the pulmonary endothelial phenotype have not been extensively studied. We cultured human pulmonary microvascular endothelial cells (HPMEC) in normoxia or hypoxia while subjected to physiological shear stress or in static conditions. Unbiased proteomics was used to identify hypoxia-induced changes in protein expression. Using publicly available single cell RNA-seq datasets, differences in gene expression between the alveolar endothelial cells from COPD and healthy lungs were identified. 60 proteins were identified in HPMEC lysates whose expression changed in response to hypoxia in sheared but not in static conditions. mRNA for five of these (ERG, MCRIP1, EIF4A2, HSP90AA1 and DNAJA1) showed similar changes in the endothelial cells of COPD compared to healthy lungs. These data show that the proteomic responses of the pulmonary microvascular endothelium to hypoxia are significantly altered by shear stress and suggest that these differences are important in the development of hypoxic pulmonary vascular disease.
2023-02-17 | PXD036260 | Pride
Project description:This study employed Affymetrix GeneChips to profile transcriptome of human pulmonary microvascular endothelial cells (HMVEC-L) treated with PBEFsiRNA to gain insight into transcriptional regulations of PBEF on the endothelial function. We isolated and labeled mRNAs from PBEF siRNA transfected HMVEC-L and hybridized them to Affymetrix GeneChip HG-U133 plus 2. Differentially expressed genes and canonical pathways were analyzed. Expressions of selected genes were validated by RT-PCR or western blotting. Several important themes are emerged from this study. First, PBEF induces the upregulation and downregulation of multiple genes in the endothelium. Expression of 373 genes were increased and 64 genes decreased by at least 1.3 fold in the PBEFsiRNA treated group compared to the control group of PBEFscRNA treated HMVEC-L. Second, the microarray results confirmed some previous reports of PBEF mediated gene expressions in some pathways but provided a more complete repertoire of molecules in those pathways. Third, most of affected canonical pathways or differentially expressed genes in PBEF siRNA treated HMVEC-L over their controls have not previously been reported to be PBEF-responsive. Our first transcriptome analysis of human pulmonary microvascular endothelial cells treated with PBEFsiRNA has provided important insights into the transcriptional regulation of gene expression in HMVEC-L cells by PBEF. Further in-depth follow-up analysis of the transcriptional regulation reported in this study may shed light on molecular mechanisms underlying PBEF mediated endothelial functions and dysfunctions in the physiology and the pathogenesis of inflammatory conditions, cancer, diabetes, coronary heart disease and provide new leads of therapeutic targets to those diseases. 6 sample microarray study - 3 replicates of the PBEF knockdown and 3 replicates of the SC RNA.
2013-01-01 | E-GEOD-34512 | biostudies-arrayexpress