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Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE234544 | GEO | 2024/04/12

REPOSITORIES: GEO

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Long non-coding RNA MEG3 promotes angiogenesis by directly regulating integrin signaling impairing endothelial cell function

Project description:We depleted MEG3-lncRNA using GapmeRs in primary human ECs. Total MEG3-regulated targets were obtained.

2024-04-12 | GSE253830 | GEO

Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIP-seq]

Project description:We immunoprecipitated EZH2, together with associated chromatin isolated from the HUVECs (2 x 10^6) that were transfected with MEG3 GapmeRs (10 nM, 48 h) or a scrambled control GapmeRs (Ctr). For transfection, we used 10 nM scrambled LNA (locked nucleic acids) GapmeR control (Cat. No. 339515) or phosphorothioate antisense standard GapmeRs MEG3-lncRNA (Cat No. 339511, Qiagen). On beads crosslinked chromatin complexes were reversed, and DNA purified using QIAquick® PCR Purification Kit and quantified by Qubit HS assay (Q33230)

2024-04-12 | GSE234543 | GEO

Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIRP-seq]

Project description:We profiled MEG-DNA interactions using gluteraldehyde assisted chromatin immunoprecipitation by RNA purification (ChIRP-seq) in primary human ECs. Genome-wide MEG3-associated loci were obtained.

2024-04-12 | GSE234542 | GEO

Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function.

Project description:Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function.

| PRJNA981989 | ENA

Long non-coding RNA MEG3 promotes angiogenesis by directly regulating integrin signaling impairing endothelial cell function

Project description:Long non-coding RNA MEG3 promotes angiogenesis by directly regulating integrin signaling impairing endothelial cell function

| PRJNA1067354 | ENA

Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIRP-seq]

Project description:Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIRP-seq]

| PRJNA981999 | ENA

Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIP-seq]

Project description:Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIP-seq]

| PRJNA982001 | ENA

Histone H3K27 methyltransferase EZH2 interacts with MEG3-lncRNA to directly regulate integrin signaling and endothelial cell function

Project description:We profiled EZH2-RNA interactions using formaldehyde/UV assisted cross-linking ligation and sequencing of hybrids (FLASH-seq) in primary human ECs. Transcriptome-wide EZH2-associated ncRNAs and RNA–RNA interactome were obtained.

2024-04-12 | GSE230112 | GEO

LncRNA Meg3 protects endothelial function by regulating the DNA damage response.

Project description:The role of long non-coding RNAs (lncRNAs) in regulating endothelial function through the DNA damage response (DDR) remains poorly understood. In this study, we demonstrate that lncRNA maternally expressed gene 3 (Meg3) interacts with the RNA binding protein polypyrimidine tract binding protein 3 (PTBP3) to regulate gene expression and endothelial function through p53 signaling ─ a major coordinator of apoptosis and cell proliferation triggered by the DDR. Meg3 expression is induced in endothelial cells (ECs) upon p53 activation. Meg3 silencing induces DNA damage, activates p53 signaling, increases the expression of p53 target genes, promotes EC apoptosis, and inhibits EC proliferation. Mechanistically, Meg3 silencing reduces the interaction of p53 with Mdm2, induces p53 expression, and promotes the association of p53 with the promoters of a subset of p53 target genes. PTBP3 silencing recapitulates the effects of Meg3 deficiency on the expression of p53 target genes, EC apoptosis and proliferation. The Meg3-dependent association of PTBP3 with the promoters of p53 target genes suggests that Meg3 and PTBP3 restrain p53 activation. Our studies reveal a novel role of Meg3 and PTBP3 in regulating p53 signaling and endothelial function, which may serve as novel targets for therapies to restore endothelial homeostasis.

| S-EPMC6379667 | biostudies-literature

Long non-coding RNA MEG3 mediates high glucose-induced endothelial cell dysfunction.

Project description:Long noncoding RNAs (lncRNAs) are implicated in the progression of diabetes mellitus (DM) and diabetes-induced endothelial dysfunction. Maternally expressed gene 3 (MEG3) encodes an lncRNA which is suggested to function as a tumor suppressor. Therefore, the aim of the present study was to investigate whether MEG3 is a potential regulator and molecular biomarker of high glucose-induced endothelial dysfunction. LncRNA Meg3-specific small interfering RNA (siRNA) and scrambled (Scr) siRNA were transfected for MEG3 dysfunction studies. RNA and protein expression were examined by quantitative RT-PCR (qPCR) and Western blot, respectively. The percentage of apoptotic cells was measured by flow cytometry. Cell viability was determined through MTT assay. This study demonstrates involvement of lncRNA MEG3 in high glucose-induced endothelial dysfunction. MEG3 is significantly downregulated in an endothelial cell model of hyperglycemia. In addition, MEG3 knockdown could exacerbate inflammatory damage in endothelial cells. Interestingly, MEG3 knockdown in HUVECs significantly induced proliferation and inhibited apoptosis by upregulating Bcl-2 and downregulating Bax, caspase-3, and P53. It should be noted that MEG3 knockdown could activate the TGF-β signaling pathway via upregulating TGF-β1, SMAD2, and SMAD7 and activate the Wnt/β-catenin signaling pathway via upregulating β-catenin and Cyclin D1 and downregulating TCF7L2. Our results indicate that MEG3 can be regarded as a novel therapeutic target and molecular biomarker for high glucose-induced endothelial dysfunction.

| S-EPMC6958101 | biostudies-literature

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