Different effects of catechin on angiogenesis and inflammation depending on VEGF levels

Negrão, Rita; Costa, Raquel; Duarte, Delfim; Taveira-Gomes, Tiago; Azevedo, Isabel; Soares, Raquel

doi:10.1016/j.jnutbio.2011.12.011

Cited by 40 publications

(27 citation statements)

References 42 publications

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“…20 Plugs placed onto GIT1-knockout (KO) mice clearly exhibited fewer vessels compared with GIT1-wild type (WT) after 7 days of incubation (Figure 1A). Also, hematoxylin and eosin staining showed fewer EC in the matrigel plugs of GIT1-KO implants compared with GIT1-WT (Figure 1A).…”

Section: Resultsmentioning

confidence: 99%

G-Protein–Coupled Receptor-2–Interacting Protein-1 Is Required for Endothelial Cell Directional Migration and Tumor Angiogenesis via Cortactin-Dependent Lamellipodia Formation

Majumder

Sowden

Gerber³

et al. 2014

ATVB

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Objective Recent evidence suggests G-protein–coupled receptor-2–interacting protein-1 (GIT1) overexpression in several human metastatic tumors, including breast, lung, and prostate. Tumor metastasis is associated with an increase in angiogenesis. We have showed previously that GIT1 is required for postnatal angiogenesis during lung development. However, the functional role of GIT1 in pathological angiogenesis during tumor growth is unknown. Approach and Results In the present study, we show inhibition of angiogenesis in matrigel implants as well as reduced tumor angiogenesis and melanoma tumor growth in GIT1-knockout mice. We demonstrate that this is a result of impaired directional migration of GIT1-depleted endothelial cells toward a vascular endothelial growth factor gradient. Cortactin-mediated lamellipodia formation in the leading edge is critical for directional migration. We observed a significant reduction in cortactin localization and lamellipodia formation in the leading edge of GIT1-depleted endothelial cells. We specifically identified that the Spa homology domain (aa 250–420) of GIT1 is required for GIT1–cortactin complex localization to the leading edge. The mechanisms involved extracellular signal-regulated kinases 1 and 2–mediated Cortactin-S405 phosphorylation and activation of Rac1/Cdc42. Finally, using gain of function studies, we show that a constitutively active mutant of cortactin restored directional migration of GIT1-depleted cells. Conclusion Our data demonstrated that a GIT1–cortactin association through GIT1-Spa homology domain is required for cortactin localization to the leading edge and is essential for endothelial cell directional migration and tumor angiogenesis.

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Section: Resultsmentioning

confidence: 99%

G-Protein–Coupled Receptor-2–Interacting Protein-1 Is Required for Endothelial Cell Directional Migration and Tumor Angiogenesis via Cortactin-Dependent Lamellipodia Formation

Majumder

Sowden

Gerber³

et al. 2014

ATVB

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“…Negrao et al studied the effects of catechin on angiogenic and inflammatory processes. Treatment with catechin increased viability and decreased apoptosis and proliferation of endothelial cells and vascular smooth muscle cells in vitro [58]. Chamcheu et al [59] demonstrated that delphinidin significantly Cell-free systems Antioxidant activity Free radical scavenging capacity, measured by the inhibition of stable radicals: DPPH (2,2-diphenyl-1-picrylhydrazyl), ABTS (2,2 0 -azino-bis(3-ethylbenzothiazoline-6-sulphonic acid)), peroxynitrite (ONOO À ), superoxide anion (O À2 ), hydroxyl radicals [8,9,16,25,[27][28][29][30][31] Oxygen radical absorbance capacity (ORAC) assay; superoxide dismutase (SOD) assay; ferric reducing antioxidant potential (FRAP) assay [16] Inhibition of lipid oxidation (liposomes, thermal acceleration of oils) [ Anti-bacterial, anti-fungal, antiviral activity [8,28,47,48] enhanced keratinocyte differentiation of NHEKs, but do not induce their apoptosis.…”

Section: Effect Of Polyphenols On the Cell Viabilitymentioning

confidence: 97%

Polyphenols as active ingredients for cosmetic products

Zillich

Schweiggert‐Weisz

Eisner

et al. 2015

Intern J of Cosmetic Sci

245

188

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Polyphenols are secondary plant metabolites with antioxidant, anti-inflammatory and anti-microbial activity. They are ubiquitously distributed in the plant kingdom; high amounts contain, for example, green tea and grape seeds. Polyphenolic extracts are attractive ingredients for cosmetics and pharmacy due to their beneficial biological properties. This review summarizes the effects of polyphenols in the context of anti-ageing activity. We have explored in vitro studies, which investigate antioxidant activity, inhibition of dermal proteases and photoprotective activity, mostly studied using dermal fibroblasts or epidermal keratinocytes cell lines. Possible negative effects of polyphenols were also discussed. Further, some physicochemical aspects, namely the possible interactions with emulsifiers and the influence of the cosmetic formulation on the skin delivery, were reported. Finally, few clinical studies, which cover the anti-ageing action of polyphenols on the skin after topical application, were reviewed.

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“…Similar results were observed by Negrao et al, who reported that 1 µM of catechin was able to reduce migration and invasion capacity in smooth muscle cells. This latter effect seems to depend on the presence or absence of angiogenesis stimuli, such as VEGF, emphasizing a potential use of some phenolic compounds against pathological situations where angiogenesis is stimulated [44]. Also, Calabriso et al demonstrated that 0.1 µg mL −1 to 10 µg mL −1 of olive oil polyphenol extract suppressed endothelial cell migration induced by VEGF.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Adhesion Process, E-Selectin and VEGF Production by Anthocyanins and Their Metabolites in an In Vitro Model of Atherosclerosis

et al. 2020

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The present study aims to evaluate the ability of peonidin and petunidin-3-glucoside (Peo-3-glc and Pet-3-glc) and their metabolites (vanillic acid; VA and methyl-gallic acid; MetGA), to prevent monocyte (THP-1) adhesion to endothelial cells (HUVECs), and to reduce the production of vascular cell adhesion molecule (VCAM)-1, E-selectin and vascular endothelial growth factor (VEGF) in a stimulated pro-inflammatory environment, a pivotal step of atherogenesis. Tumor necrosis factor-α (TNF-α; 100 ng mL −1 ) was used to stimulate the adhesion of labelled monocytes (THP-1) to endothelial cells (HUVECs). Successively, different concentrations of Peo-3-glc and Pet-3-glc (0.02 µM, 0.2 µM, 2 µM and 20 µM), VA and MetGA (0.05 µM, 0.5 µM, 5 µM and 50 µM) were tested. After 24 h, VCAM-1, E-selectin and VEGF were quantified by ELISA, while the adhesion process was measured spectrophotometrically. Peo-3-glc and Pet-3-glc (from 0.02 µM to 20 µM) significantly (p < 0.0001) decreased THP-1 adhesion to HUVECs at all concentrations (−37%, −24%, −30% and −47% for Peo-3-glc; −37%, −33%, −33% and −45% for Pet-3-glc). VA, but not MetGA, reduced the adhesion process at 50 µM (−21%; p < 0.001). At the same concentrations, a significant (p < 0.0001) reduction of E-selectin, but not VCAM-1, was documented. In addition, anthocyanins and their metabolites significantly decreased (p < 0.001) VEGF production. The present findings suggest that while Peo-3-glc and Pet-3-glc (but not their metabolites) reduced monocyte adhesion to endothelial cells through suppression of E-selectin production, VEGF production was reduced by both anthocyanins and their metabolites, suggesting a role in the regulation of angiogenesis.

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Different effects of catechin on angiogenesis and inflammation depending on VEGF levels

Cited by 40 publications

References 42 publications

G-Protein–Coupled Receptor-2–Interacting Protein-1 Is Required for Endothelial Cell Directional Migration and Tumor Angiogenesis via Cortactin-Dependent Lamellipodia Formation

G-Protein–Coupled Receptor-2–Interacting Protein-1 Is Required for Endothelial Cell Directional Migration and Tumor Angiogenesis via Cortactin-Dependent Lamellipodia Formation

Polyphenols as active ingredients for cosmetic products

Modulation of Adhesion Process, E-Selectin and VEGF Production by Anthocyanins and Their Metabolites in an In Vitro Model of Atherosclerosis

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