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

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 655 ◽  
Author(s):  
Mirko Marino ◽  
Cristian Del Bo’ ◽  
Massimiliano Tucci ◽  
Dorothy Klimis-Zacas ◽  
Patrizia Riso ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Vitro Model ◽  
Vascular Endothelial ◽  
Tnf Α ◽  
Vitro Model ◽  
Factor Α ◽  
Endothelial Growth Factor ◽  
Adhesion Process ◽  
Necrosis Factor

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.

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

2020 ◽  
Author(s):  
Mirko Marino ◽  
Cristian Del Bo’ ◽  
Massimiliano Tucci ◽  
Dorothy Klimis-Zacas ◽  
Patrizia Riso ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Vanillic Acid ◽  
Tumor Necrosis ◽  
In Vitro Model ◽  
Monocyte Adhesion ◽  
Vitro Model ◽  
Adhesion Process ◽  
Necrosis Factor

The present study aims to evaluate the ability of peonidin and petunidin-3-glucoside (Peo 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 VCAM-1, E-selectin and VEGF in a stimulated pro-inflammatory environment, a pivotal step of atherogenesis. Tumor necrosis factor-&alpha; (TNF-&alpha;; 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, 0.2, 2 and 20 &micro;M) and VA and MetGA (0.05, 0.5, 5 and 50 &micro;M) were tested. After 24 h, the production of VCAM-1, E-selectin and VEGF was quantified by ELISA kits, while the adhesion process was measured spectrophotometrically. Peo-3-glc and Pet-3-glc (from 0.02 to 20 &micro;M) significantly (p&lt;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 &micro;M (-21%; p&lt;0.001). At the same concentrations, a significant (p&lt;0.0001) reduction of E-selectin, but not VCAM-1, was documented. In addition, anthocyanins and their metabolites significantly decreased (p&lt;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 regulation of angiogenesis.

Influence of cytokines and growth factors in ANG II-mediated collagen upregulation by fibroblasts in rats: role of myocytes

2004 ◽  
Vol 287 (1) ◽  
pp. H107-H117 ◽  
Author(s):  
Sagartirtha Sarkar ◽  
Elangovan Vellaichamy ◽  
David Young ◽  
Subha Sen
Keyword(s):  
In Vitro Model ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Ang Ii ◽  
Tnf Α ◽  
Paracrine Action ◽  
Vitro Model ◽  
Necrosis Factor

Abnormal stiffness and altered cardiac function arising from abnormal collagen deposition occur in hypertrophy and heart failure. ANG II has been shown to play a role in this process. To evaluate the mechanism, we developed an in vitro model by subjecting fibroblasts to ANG II treatment in the presence or absence of myocytes in coculture ( 25 ). Employing this model, we demonstrated that ANG II-induced collagen gene transcription in cardiac fibroblasts was potentiated by myocyte-derived factors. In attempting to identify mechanisms of collagen upregulation and to define the role of myocytes, we found that interleukin (IL)-6, tumor necrosis factor (TNF)-α, and the transforming growth factor (TGF)-β superfamily were also involved in collagen upregulation. Collagen transcripts were increased after fibroblasts were treated with IL-6 (20–50 ng/ml) and TNF-α (0.1–0.5 ng/ml). In this study, we show that cardiomyocytes induce secretion of active TGF-β in the presence of ANG II and that a paracrine action of TGF-β subsequently induces different cytokines (IL-6) in fibroblasts, thereby promoting collagen synthesis. The cross-talk between myocytes and fibroblasts and involvement of these cytokines in the upregulation of collagen transcript levels are novel findings that may explain their possible roles in the upregulation of collagen.

scholarly journals In vitro model of distinct catabolic and inflammatory response patterns of endothelial cells to intervertebral disc cell degeneration

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Min Ho Hwang ◽  
Hyeong-Guk Son ◽  
Joohan Kim ◽  
Hyuk Choi
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Intervertebral Disc ◽  
Vascular Endothelial ◽  
Response Patterns ◽  
Cell Degeneration ◽  
Microfluidic Platform ◽  
Vitro Model ◽  
Endothelial Growth Factor

AbstractTo evaluate dominant cell-to-cell paracrine interactions, including those of human annulus fibrosus (AF), nucleus pulposus (NP), and endothelial cells (ECs), in the production of inflammatory mediators and catabolic enzymes, ECs was cultured in soluble factors derived from AF or NP cells (AFCM or NPCM, respectively) and vice versa. We analysed IL-6 and -8, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-1 and -3, nerve growth factor (NGF)-β, and brain-derived neurotrophic factors (BDNFs) with qRT-PCR and ELISA. We implement a microfluidic platform to analyse migration properties of AF and NP cells and ECs in 3D cultures. Our results show that IL-1β-stimulated AF cells produced significantly higher levels of IL-6 and -8, VEGF, and MMP-1 than IL-1β-stimulated NP cells. However, production of IL-6 and -8, VEGF, and MMP-3 was significantly higher in NP cells than in AF cells, under the presence of ECs conditioned medium. We observed considerable migration of NP cells co-cultured with ECs through the microfluidic platform. These results suggest that AF cells may play a major role in the initial degeneration of intervertebral disc. Furthermore, it was found that interactions between NP cells and ECs may play a significant role in the development or progression of diseases.

An in vitro model for the study of microglia-induced neurodegeneration: involvement of nitric oxide and tumor necrosis factor-α

2001 ◽  
Vol 38 (7) ◽  
pp. 557-565 ◽  
Author(s):  
Karin Hemmer ◽  
Lucie Fransen ◽  
Hugo Vanderstichele ◽  
Eugeen Vanmechelen ◽  
Paul Heuschling
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
In Vitro Model ◽  
Vitro Model ◽  
Factor Α ◽  
Necrosis Factor
Sign in / Sign up

Export Citation Format

Share Document