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Exploring the molecular mechanism and and related signaling pathways of annexin A2 in human retinal vascular endothelial cells

ABSTRACT: To investigate the role and mechanism of ANXA2 in retinal neovascularization, we used interfering and overexpressing lentivirus to intervene in HREC cells, respectively. Divided into interference group (negative control group and positive interference group), overexpression group (negative control group, overexpression positive control group). The mechanism of action of annexin A2 in human retinal vascular endothelium was explored by real-time PCR to quantify the expression of molecular genes in samples.

ORGANISM(S): Homo sapiens

PROVIDER: GSE136120 | GEO | 2022/08/20

REPOSITORIES: GEO

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Role of annexin A2 in muscle repair

Project description:Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.

2016-10-04 | GSE87557 | GEO

Activation of YAP-dependent Proliferation by a Small Molecule Targeting Annexin A2

Project description:The transcriptional coactivator YAP orchestrates a pro-proliferative transcriptional program that controls the fate of somatic stem cells and the regenerative responses of certain tissues. As such, agents that activate YAP may hold therapeutic potential in disease states exacerbated by insufficient proliferative repair. Here we report the discovery of a small molecule, termed PY-60, which robustly activates YAP transcriptional activity in vitro and promotes YAP-dependent expansion of epidermal keratinocytes in mouse upon topical administration of drug. Chemical proteomics revealed the relevant target of PY-60 to be Annexin A2 (ANXA2), a protein that directly associates with YAP at the cell membrane in response to increased cell density. PY-60 treatment liberates ANXA2 from the membrane, ultimately promoting a phosphatase bound, non-phosphorylated, and transcriptionally active form of YAP. This work reveals ANXA2 to be a previously undescribed, druggable component of the Hippo pathway and suggests a mechanistic rationale for promoting YAP-dependent regenerative repair in disease.

2021-01-14 | GSE164801 | GEO

Annexin A2 Modulates Radiation-Sensitive Transcriptional Programming and Cell Fate

Project description:Whole genome expression profiling in the presence and absence of annexin A2 [shRNA] identified fundamentally altered transcriptional programming that changes the radioresponsive transcriptome. Bioinformatics predicted that silencing AnxA2 may enhance cell death responses to stress in association with reduced activation of pro-survival signals such as nuclear factor kappa B. This prediction was validated by demonstrating a significant increase in sensitivity toward tumor necrosis factor alpha induced cell death in annexin A2 silenced cells, relative to vector controls, associated with reduced nuclear translocation of RelA (p65) following tumor necrosis factor alpha treatment. Murine progenitor cells, JB6 cell line, were stably transformed with Annexin A2 shRNA or vector only control and then treated with ionizing radiation at two doses, 10cGy and 100cGy. Samples were collected at 2hr, 6hr and 24hr for RNA isolation. Two untreated time points were collected also: 2hr and 24hr.

2012-11-28 | E-GEOD-42547 | biostudies-arrayexpress

Annexin A2 Modulates Radiation-Sensitive Transcriptional Programming and Cell Fate

2012-11-28 | GSE42547 | GEO

Annexin 2A sustains glioblastoma cell dissemination and proliferation affecting patient prognosis

Project description:Glioblastoma (GBM) is the most devastating tumour of the brain, endowed with a fatal prognosis. Indeed, the complete eradication of cancer cell disseminated outside the GBM mass still remains a crucial issue. Given the reported strong association existing between Annexin 2A (ANXA2) expression and cell dissemination in many cancers, we evaluated the effects exerted by the modulation of ANXA2 levels in GBM cells and assessed its potential in predicting patient outcome. Here, we show that expression of ANXA2 positively correlates with metastatic gene signatures and demonstrates to be prognostic by itself. Indeed, we prove that ANXA2 is involved in cell migration, invasion, cytoskeletal remodeling and proliferation in GBM cells. Moreover, we were able to construct a gene signature representative of ANXA2 inhibition, which showed a significant prognostic potential in different GBM patient cohorts. In this study, we demonstrate that ANXA2 acts at multiple levels in determining the disseminating and aggressive behaviour of GBM tumours. In particular, we clearly show that ANXA2 is involved in determining a migrating and disseminating phenotype of GBM cells, in controlling specific cell cycle checkpoints and a cytoskeletal remodeling associated to cell movement. These data sustain the potential of ANXA2 as a possible target and strong prognostic factor in the future management of GBM patients. Gene expression was measured on Affymetrix in 4 independent experiments of primary GBM cells treated with an ANXA2 neutralizing antibody

2016-07-24 | E-GEOD-76786 | biostudies-arrayexpress

Annexin 2A sustains glioblastoma cell dissemination and proliferation affecting patient prognosis

2016-07-24 | GSE76786 | GEO

Annexin A2 controls pancreatic cancer invasion and metastasis through a novel axon guidance pathway

Project description:The mechanisms involved in promoting metastasis of pancreatic ductal adenocarcinoma have yet to be elucidated. Here, we show that AnnexinA2 regulates the secretion of Semaphorin3D from pancreatic tumor cells allowing it to bind to its receptor PlexinD1 on the surface of the tumor cell, which induces invasion and metastasis. Knockdown of AnnexinA2 or Semaphorin3D decreases the metastatic potential of pancreatic tumor cells, while over expression of AnnexinA2 or Semaphorin3D is sufficient to rescue the invasion capacity of these cells. Clinically, we found that Semaphorin3D expression correlates with poor survival and increased metastatic potential in human PDA patients. This study identified a novel axon guidance pathway downstream of AnnexinA2 that can be targeted in the treatment of metastatic pancreatic cancer. Two primary pancreatic tumor cell lines were analyzed. The first primary line was derived from a KrasG12D/p53172H/Pdx-1Cre mouse, which served as the reference sample. The second primary line was derived from a KrasG12D/p53R172H/Pdx-1Cre/AnxA2-/- mouse.

2015-09-03 | E-GEOD-62285 | biostudies-arrayexpress

Genotoxic agents promote the nuclear accumulation of annexin A2: role of annexin A2 in mitigating DNA damage.

Project description: Not available

| S-EPMC3511559 | biostudies-literature

Membrane Binding Promotes Annexin A2 Oligomerization.

Project description: Not available

| S-EPMC7291239 | biostudies-literature

Gene expression data from AP-2γ silenced MCF-7 cells

Project description:Overexpression of the AP-2γ transcription factor in breast tumours has been identified as an independent predictor of poor outcome and failure of hormone therapy, even in ER positive, ErbB2 negative tumours; markers of a more favourable prognosis. To understand further the role of AP-2γ in breast carcinoma, we have used an RNA interference and gene expression profiling strategy using the MCF-7 cell line as a model for ER positive, ErbB2 negative tumours with AP-2γ overexpression. Gene expression changes between control and silenced cells implicate AP-2γ in the control of cell cycle progression and developmental signalling. Keywords: RNA interference

2009-12-14 | GSE15481 | GEO

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