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NcRNA (non-coding RNA) signature in endothelial cells during hypoxia [RNA-seq]

ABSTRACT: To define ncRNA expression in hypoxic endothelial cells, we applied pro-angiogenic hypoxia to cultured endothelial cells. Afterwards, total RNA was isolated and underwent RNA-seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE70330 | GEO | 2015/07/01

SECONDARY ACCESSION(S): PRJNA288326

REPOSITORIES: GEO

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ncRNA (non-coding RNA) signature in endothelial cells during hypoxia

Project description:To define ncRNA expression in hypoxic endothelial cells, we applied pro-angiogenic hypoxia to cultured endothelial cells. Afterwards total RNA was isolated and underwent genechip analysis. HUVECs were subjected to normoxic or hypoxic (0.1-0.2% O2) cell culture conditions.

2015-06-25 | E-GEOD-70034 | biostudies-arrayexpress

ncRNA (non-coding RNA) signature in endothelial cells during hypoxia [RNA-seq]

Project description:To define ncRNA expression in hypoxic endothelial cells, we applied pro-angiogenic hypoxia to cultured endothelial cells. Afterwards, total RNA was isolated and underwent RNA-seq analysis. HUVECs were subjected to normoxic or hypoxic (0.1-0.2% O2) cell culture conditions.

2015-07-01 | E-GEOD-70330 | biostudies-arrayexpress

ncRNA (non-coding RNA) signature in endothelial cells during hypoxia [array]

2015-06-25 | GSE70034 | GEO

Hypoxia-induced proteomic remodeling of human mammary cancer associated fibroblast - siRNA NCBP2-AS2

Project description:Intratumoral hypoxia causes the formation of dysfunctional blood vessels which contribute to tumor metastasis. Blood vessels are embedded in the tumor stroma where cancer-associated fibroblasts (CAFs) constitute the most prominent cellular component. We found that hypoxic human mammary CAFs promote blood vessel growth in CAF-endothelial cell co-cultures in vitro. Mass spectrometry-based proteomic analysis of CAF secretome unravels how hypoxic CAFs contribute to blood vessel abnormalities by altering the secretion of a multitude of pro- and anti-angiogenic factors. Hypoxia induces pronounced remodeling of the CAF proteome, including proteins that have not been previously related to this process. Amongst those, the uncharacterized antisense gene protein NCBP2-AS2 is one of the most transcriptionally upregulated proteins in the proteome and secretome of hypoxic CAFs. Silencing of NCBP2-AS2 abrogates the pro-angiogenic function acquired by hypoxic CAFs through decreasing VEGF expression levels to the levels found in normoxic CAFs.

2019-02-15 | PXD006539 | Pride

Hypoxia-induced ncRNA transcriptome in TNBC cells

Project description:Whole transcriptome sequencing was performed to identify ncRNA transcriptome in two human TNBC cell lines under normoxia and hypoxia

2021-06-17 | GSE144569 | GEO

Hypoxia-induced proteomic remodeling of human mammary cancer associated fibroblast

Project description:Intratumoral hypoxia causes the formation of dysfunctional blood vessels which contribute to tumor metastasis. Blood vessels are embedded in the tumor stroma where cancer-associated fibroblasts (CAFs) constitute the most prominent cellular component. We found that hypoxic human mammary CAFs promote blood vessel growth in CAF-endothelial cell co-cultures in vitro. Mass spectrometry-based proteomic analysis of CAF secretome unravels how hypoxic CAFs contribute to blood vessel abnormalities by altering the secretion of a multitude of pro- and anti-angiogenic factors. Hypoxia induces pronounced remodeling of the CAF proteome, including proteins that have not been previously related to this process. Our study provides a map of unprecedented depth of hypoxia-induced molecular alterations in mammary CAFs that can be exploited to identify novel mechanisms that control hypoxic CAF functions.

2019-02-15 | PXD006535 | Pride

Long non-coding RNA Neat1 is a key of translational regulator in hypoxia

Project description:Internal ribosome entry sites (IRESs) drive translation initiation during stress. In response to hypoxia, (lymph)angiogenic factors responsible for tissue revascularization in ischemic diseases are induced by the IRES-dependent mechanism. Here we searched for IRES trans-acting factors (ITAFs) active in early hypoxia in mouse cardiomyocytes. Using knock-down and proteomics approaches, we show a link between a stressed-induced nuclear body, the paraspeckle, and IRES-dependent translation. Our data reveal that the long non-coding RNA Neat1, an essential paraspeckle component, is a key translational regulator, active on IRESs of (lymph)angiogenic and cardioprotective factor mRNAs. In addition, paraspeckle proteins p54nrb and PSPC1 as well as nucleolin and Rps2, two p54nrb-interacting proteins identified by mass spectrometry, are ITAFs for IRES subgroups. Paraspeckle thus appears as the site of IRESome assembly in the nucleus. Polysome PCR array showed that the Neat1_2 isoform widely affects translation of mRNAs containing IRESs, involved in stress response, angiogenesis or cardioprotection.

2023-01-03 | PXD024067 | Pride

Hypoxia-induced ncRNA transcriptome in TNBC cells

Project description:Hypoxia-induced ncRNA transcriptome in TNBC cells

| PRJNA604033 | ENA

Discovery of RUF6 ncRNA interacting proteins involved in P. falciparum immune evasion

Project description:RUF6 is a ncRNA gene family that is transcribed by RNA Polymerase III but actively regulates the Pol II-transcribed var virulence gene family. Understanding how RUF6 ncRNA connect to downstream effectors is lacking. We developed an RNA-directed proteomic discovery (ChIRP-MS) protocol to identify in vivo RUF6 ncRNA protein interactions. The RUF6 ncRNA interactome was purified with biotinylated antisense oligonucleotides. Quantitative label-free mass spectrometry identified several unique proteins linked to gene transcription including. Affinity purification of Pf-DDX5 identified proteins originally found by our RUF6-ChIRP protocol, validating the technique’s robustness for identifying ncRNA interactomes in P. falciparum. Our work identifies a RUF6 ncRNA protein complex that interacts with RNA Pol II to sustain var gene expression.

2022-11-15 | PXD036801 | Pride

Mir-130a potentiates the reparative properties of human endothelial colony forming cells facing hypoxia via VEGFR2 and STAT3

Project description:Hypoxia controls reparative angiogenesis. MiRNAs are master regulators of gene expression in hypoxia and angiogenesis. However, we do not yet have a clear understanding of how hypoxia-induced miRNAs modulate vasoreparative processes. Here, we identify miR-130a as a mediator of the hypoxic response in human primary endothelial colony forming cells (ECFCs), a well-characterized subtype of endothelial progenitor. Under hypoxic conditions, miR-130a overexpression enhances ECFC pro-angiogenic capacity in vitro and potentiates their vasoreparative properties in vivo. Mechanistically, miR-130a orchestrates upregulation of VEGFR2, activation of STAT3-dependent transcription, and accumulation of HIF1α via translational inhibition of DDX6. These findings unveil a new role for miR-130a in hypoxia, whereby it modulates the VEGFR2/STAT3/HIF1α axis to increase the vasoregenerative capacity of ECFCs.

2022-12-06 | GSE142123 | GEO

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