Caveolin-1 Down-Regulation Reduces VEGF-A Secretion Induced by IGF-1 in ARPE-19 Cells

Puddu, Alessandra; Sanguineti, Roberta; Maggi, Davide

doi:10.3390/life12010044

Cited by 9 publications

(3 citation statements)

References 31 publications

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“…Specifically, the authors found that down-regulation of CAV-1 reduced constitutive VEGF-A secretion and insulin-like growth factor 1 (IGF-1)-stimulated VEGF-A release. [42] A similar phenomenon was also demonstrated in pancreatic cell lines, in which knockdown of CAV-1 increased insulin secretion under physiological glucose levels. [43] The loss of CAV-1 expression, associated with the disruption of caveolae, was likely linked to the impaired secretion VEGF-A angiogenic factors, suggesting a role of CAV-1 in regulating VEGF-A secretion.…”

Section: Discussionsupporting

confidence: 56%

VEGF‐R2/CAV‐1 Interaction Induced by Resveratrol/Eicosapentaenoic Acid/Docosahexaenoic Acid‐Enriched Formulation through Functional Detergent‐Resistant Membranes Is Associated with Decreased VEGF‐A Release in ARPE‐19 Cells

Perus,

Courtaut,

Pais de Barros

et al. 2024

Molecular Nutrition Food Res

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ScopeOmega‐3 fatty acids (O3FAs) and resveratrol (RSV) are known to be beneficial for certain eye diseases, such as age‐related macular degeneration (AMD). Neovascular AMD is characterized by abnormal blood vessel formation due to the excessive synthesis of vascular endothelial growth factor (VEGF) by retinal pigment epithelium (RPE) cells. The study investigates whether a formulation based on eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and RSV is capable of counteracting VEGF‐A secretion, and elucidates the molecular mechanism.Methods and resultsThe study finds, using ELISA, that O3FAs/RSV reduces VEGF‐A secretion in human RPE cells. This phenomenon is related to the increased interaction between VEGF‐receptor 2 (VEGF‐R2) and caveolin‐1 (CAV‐1), a protein of detergent‐resistant membranes (DRMs), as determined by co‐immunoprecipitation and proximity ligation assay. Using microscale thermophoresis, the study confirms that O3FAs/RSV causes a high‐affinity interaction. Isolation and analysis of DRMs reveal that this interaction is concomitant with VEGF‐R2 relocalization in DRMs. The depletion of DRMs by a cholesterol‐chelating agent blocks the VEGF‐R2/CAV‐1 interaction and EPA/DHA/RSV‐mediated impairment of VEGF production.ConclusionThis specific interaction can provide a new strategy for countering VEGF‐A production in human RPE cells and, consequently, reducing neovascularization in AMD. Further preclinical studies involving O3FAs and polyphenols are warranted.

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Section: Discussionsupporting

confidence: 56%

VEGF‐R2/CAV‐1 Interaction Induced by Resveratrol/Eicosapentaenoic Acid/Docosahexaenoic Acid‐Enriched Formulation through Functional Detergent‐Resistant Membranes Is Associated with Decreased VEGF‐A Release in ARPE‐19 Cells

Perus,

Courtaut,

Pais de Barros

et al. 2024

Molecular Nutrition Food Res

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“… 42 , 43 Furthermore, as a major marker of caveolae in endothelial cells, CAV1 are increasing expressed by HIV infection and also interacts with a lot of intracellular signaling molecules such as MAPK and VEGFA. 44 - 46 Therefore, the real functions of these core genes in COVID-19 patients are worthy of investigating and validating in the future.…”

Section: Discussionmentioning

confidence: 99%

The Biological Processes of Ferroptosis Involved in Pathogenesis of COVID-19 and Core Ferroptoic Genes Related With the Occurrence and Severity of This Disease

Zhang

Pang

et al. 2023

Evol Bioinform Online

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Background: A worldwide outbreak of coronavirus disease 2019 (COVID-19) has resulted in millions of deaths. Ferroptosis is a form of iron-dependent cell death which is characterized by accumulation of lipid peroxides on cellular membranes, and is related with many physiological and pathophysiological processes of diseases such as cancer, inflammation and infection. However, the role of ferroptosis in COVID-19 has few been studied. Material and Method: Based on the RNA-seq data of 100 COVID-19 cases and 26 Non-COVID-19 cases from GSE157103, we identified ferroptosis related differentially expressed genes (FRDEGs, adj. P-value < .05) using the “Deseq2” R package. By using the “clusterProfiler” R package, we performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. Next, a protein-protein interaction (PPI) network of FRDEGs was constructed and top 30 hub genes were selected by cytoHubba in Cytoscape. Subsequently, we established a prediction model for COVID-19 by utilizing univariate logistic regression and the least absolute shrinkage and selection operator (LASSO) regression. Based on core FRDEGs, COVID-19 patients were identified as two clusters using the “ConsenesusClusterPlus” R package. Finally, the miRNA-mRNA network was built by Targetscan online database and visualized by Cytoscape software. Results: A total of 119 FRDEGs were identified and the GO and KEGG enrichment analyses showed the most important biologic processes are oxidative stress response, MAPK and PI3K-AKT signaling pathway. The top 30 hub genes were selected, and finally, 7 core FRDEGs (JUN, MAPK8, VEGFA, CAV1, XBP1, HMOX1, and HSPB1) were found to be associated with the occurrence of COVID-19. Next, the two patterns of COVID-19 patients had constructed and the cluster A patients were likely to be more severe. Conclusion: Our study suggested that ferroptosis was involved in the pathogenesis of COVID-19 disease and the functions of core FRDEGs may become a new research aspect of this disease.

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“…The release of VEGF-A activates a feedback loop that further enhances NF-kB activation and VEGF-A secretion. Interestingly, we previously demonstrated that Cav-1 depletion reduced basal and IGF-1-induced VEGF-A secretion in retinal pigment epithelial cells [80]. Therefore, it can be hypothesized that the absence of Cav-1 may also reduce VEGF-A secretion in endothelial cells.…”

Section: Cav-1 and Ldl Metabolismmentioning

confidence: 93%

Caveolin-1 and Atherosclerosis: Regulation of LDLs Fate in Endothelial Cells

Puddu

Montecucco

Maggi

2023

IJMS

Self Cite

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Caveolae are 50–100 nm cell surface plasma membrane invaginations observed in terminally differentiated cells. They are characterized by the presence of the protein marker caveolin-1. Caveolae and caveolin-1 are involved in regulating several signal transduction pathways and processes. It is well recognized that they have a central role as regulators of atherosclerosis. Caveolin-1 and caveolae are present in most of the cells involved in the development of atherosclerosis, including endothelial cells, macrophages, and smooth muscle cells, with evidence of either pro- or anti-atherogenic functions depending on the cell type examined. Here, we focused on the role of caveolin-1 in the regulation of the LDLs’ fate in endothelial cells.

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Caveolin-1 Down-Regulation Reduces VEGF-A Secretion Induced by IGF-1 in ARPE-19 Cells

Cited by 9 publications

References 31 publications

VEGF‐R2/CAV‐1 Interaction Induced by Resveratrol/Eicosapentaenoic Acid/Docosahexaenoic Acid‐Enriched Formulation through Functional Detergent‐Resistant Membranes Is Associated with Decreased VEGF‐A Release in ARPE‐19 Cells

VEGF‐R2/CAV‐1 Interaction Induced by Resveratrol/Eicosapentaenoic Acid/Docosahexaenoic Acid‐Enriched Formulation through Functional Detergent‐Resistant Membranes Is Associated with Decreased VEGF‐A Release in ARPE‐19 Cells

The Biological Processes of Ferroptosis Involved in Pathogenesis of COVID-19 and Core Ferroptoic Genes Related With the Occurrence and Severity of This Disease

Caveolin-1 and Atherosclerosis: Regulation of LDLs Fate in Endothelial Cells

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