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Dimethyl Fumarate (DMFu) as an anti-angiogenic agent in VEGF-treated human microvascular retinal endothelial cells (HRECs).

ABSTRACT: Dimethyl Fumarate (DMFu) as an anti-angiogenic agent in VEGF-treated human microvascular retinal endothelial cells (HRECs).

PROVIDER: PRJNA1204363 | ENA |

REPOSITORIES: ENA

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Dimethyl Fumarate (DMFu) as an anti-angiogenic agent in VEGF-treated human microvascular retinal endothelial cells (HRECs).

Project description:Vascular endothelial growth factor (VEGF) is a key driver of retinal and choroidal angiogenesis in wet age-related macular degeneration (nAMD). The present study investigated the impact of dimethyl fumarate (DMFu), a novel nAMD therapeutic candidate, on the transcriptomic profile of VEGF-treated primary human retinal endothelial cells (HRECs). In performing this study, we have described the individual transcriptomic implications of VEGF and DMFu in HRECs and characterised the impact of DMFu treatment on gene expression in VEGF-activated HRECs.

2025-09-03 | GSE285562 | GEO

Genes associated with angiogenic response to Ang-1 or VEGF

Project description:Specific Aims To identify novel transcriptional events associated with angiogenesis in VEGF and Ang-1 stimulated rat aortic rings. Our studies take advantage of the capacity of rat aortic rings to generate new vessels in collagen gels. Rat aortic rings embedded in collagen gel immediately after excision from the animal produce a self-limited angiogenic response under serum-free conditions and in the absence of exogenous stimuli. This angiogenic response can be dose-dependently promoted by vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1), which are critical regulators of the angiogenic process during embryonal development and postnatal angiogenesis. Aortic rings lose their capacity to spontaneously generate new vessels if embedded in collagen gels 10-14 days after excision. VEGF has the capacity to turn back “on” these quiescent rings producing florid angiogenesis. Conversely, Ang-1 potentiates an existing angiogenic response, but is unable to turn the quiescent system “on”. Since VEGF-mediated induction of angiogenic sprouting occurs 1-2 days of treatment, we hypothesize that this process is regulated by a unique set of “angiogenesis inducer genes” that are activated by VEGF and not by Ang-1. Identification of the proteins encoded by these genes may advance our understanding of the molecular mechanisms that regulate the earliest stages of the angiogenic cascade. Keywords: Response to growth factors

2006-03-22 | GSE3355 | GEO

Expression data of renal cancer cell treated with Oncolytic virus VSVd51 and Fumaric acid esters such as Dimethyl fumarate

Project description:We propose a strategy to boost the therapeutic efficacy of Oncolytic therapy by combining it with fumaric acid ester such as Dimethyl fumarate (DMF) The mechanism of action was examined by microarray analysis using the Affymetrix Human PrimeView Array.

2018-07-30 | GSE97328 | GEO

Extracellular vimentin mimics VEGF and is a target for anti-angiogenic immunotherapy

Project description:Anti-angiogenic anticancer therapies possess immune-stimulatory properties by counteracting pro-angiogenic molecular mechanisms. We report that tumor endothelial cells ubiquitously overexpress and secrete the intermediate filament protein vimentin through type III unconventional mechanisms. Extracellular vimentin is pro-angiogenic and functionally mimics VEGF action, while concomitantly acting as inhibitor of leukocyte-endothelial interactions. Targeting of extracellular vimentin presents a promising anti-angiogenic immunotherapy strategy against cancer. Here we describe profiling of the HUVEC (Human Umbilical Vein Endothelial Cell) proteome, with special emphasis on vimentin (variants) in the different fractions. We have evidence that vimentin is externalized and deposited in the matrix of cultured cells and is as such available for targeted antiangiogenic therapeutics. The aim of the experiment is to determine the protein variants of vimentin in the cell, the secretome, and in the matrix deposited by the cells.

2022-03-29 | PXD024426 | Pride

Chemical proteomic map of dimethyl fumarate-sensitive cysteines in primary human T cells

Project description:Primary human and mouse T cells were treated with the multiple sclerosis drug dimethyl fumarate (DMF) or its in vivo metabolite monomethyl fumarate (MMF). Cysteines sensitive to DMF or MMF were identified using iodoacetamide alkyne enrichment.

2016-08-31 | MSV000080111 | MassIVE

Differential neuroprotective and anti-inflammatory effects of dimethyl fumarate, monomethyl fumarate and cannabidiol in neurons and microglia

Project description:Dimethyl fumarate (DMF) is an immunomodulatory treatment for multiple sclerosis (MS) that can cross the blood-brain barrier, presenting neuroprotective potential. Its mechanism of action is not fully understood and there is a need to characterize if DMF or its bioactive metabolite monomethyl fumarate (MMF) exert neuroprotective properties. The combination of adjuvant agents such as cannabidiol (CBD) could be relevant to enhance neuroprotection. The aim of this study was to compare the effects of DMF, MMF and CBD on neuroprotective and immunomodulatory pathways in neurons and microglia in vitro. We found that DMF and CBD, but not MMF, activated the Nrf2 antioxidant pathway in neurons. Similarly, only DMF and CBD, but not MMF, prevented the LPS-induced activation of the inflammatory pathway NF-kB in microglia. However, the 3 drugs inhibited the production of nitric oxide in microglia and protected neurons against apoptosis. Transcriptomically, DMF, MMF and CBD exhibited differential effects on these pathways, with DMF achieving the most pronounced changes. Our results show that DMF and MMF, despite being structurally related, present differences in their mechanisms of action that could be relevant for the achievement of neuroprotection in MS patients and the potential of CBD as an adjuvant therapy in neuroprotection.

2024-09-30 | GSE274435 | GEO

Differential neuroprotective and anti-inflammatory effects of dimethyl fumarate, monomethyl fumarate and cannabidiol in neurons and microglia

Project description:Differential neuroprotective and anti-inflammatory effects of dimethyl fumarate, monomethyl fumarate and cannabidiol in neurons and microglia

| PRJNA1146415 | ENA

Differential neuroprotective and anti-inflammatory effects of dimethyl fumarate, monomethyl fumarate and cannabidiol in neurons and microglia [Mouse]

2024-09-30 | GSE274859 | GEO

Differential neuroprotective and anti-inflammatory effects of dimethyl fumarate, monomethyl fumarate and cannabidiol in neurons and microglia [Mouse]

Project description:Differential neuroprotective and anti-inflammatory effects of dimethyl fumarate, monomethyl fumarate and cannabidiol in neurons and microglia [Mouse]

| PRJNA1148203 | ENA

Circulating microRNAs in relapsing MS patients treated with dimethyl fumarate in the phase 4 TREMEND trial

Project description:Dimethyl fumarate (DMF) is an oral drug approved for relapsing multiple sclerosis (MS) that leads to reduction of neurofilament light (NFL). This may be related to dynamics and persistence of microRNA signatures in the peripheral blood of treatment-naïve MS patients before and after dimethyl fumarate (DMF) at different time points. 210 blood samples were collected from 51 treatment-naïve patients at baseline (BL) and after 1-3, 4-7, 9-15 and 21-27 months of DMF and from 22 controls from the phase IV TREMEND trial. Using microarray, 1,085 miRNAs were two-folds above the background and compared versus NFL. Altered miRNA profiles peaked after 4-7 months. MiR-16-5p and miR-4306, involved in the NF-kB-pathway, were upregulated in low NFL samples, while miR-940 and miR-4665-3p were upregulated in high NFL samples. NFL and miRNA correlations were strongest after 4-7 months DMF. In four patients with blood samples taken at all 5 time points, time-series analysis found miR-146a-5p, the inhibitor of the NF-kB-pathway, increased 1-3 months after treatment. DMF induces dynamic changes in composite miRNA profiles 4-7 months after initiation, several involved in the NF-kB-pathway. Upregulation of miR-16-5p and miR-4306 in low-NFL, while miR-940 and miR-4665-3p in high-NFL samples may indicate a response to DMF treatment.

2022-10-26 | GSE215450 | GEO

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