scholarly journals In Vivo and In Vitro Inhibition of Monocyte Adhesion to Endothelial Cells and Endothelial Adhesion Molecules by Eicosapentaenoic Acid

2008 ◽  
Vol 28 (12) ◽  
pp. 2173-2179 ◽  
Author(s):  
Hideto Yamada ◽  
Masayuki Yoshida ◽  
Yasutaka Nakano ◽  
Takayoshi Suganami ◽  
Noriko Satoh ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Eicosapentaenoic Acid ◽  
Adhesion Molecules ◽  
Monocyte Adhesion ◽  
In Vitro Inhibition ◽  
Endothelial Adhesion Molecules

scholarly journals Natural Compound Resveratrol Attenuates TNF-Alpha-Induced Vascular Dysfunction in Mice and Human Endothelial Cells: The Involvement of the NF-κB Signaling Pathway

2021 ◽  
Vol 22 (22) ◽  
pp. 12486
Author(s):  
Palanisamy Nallasamy ◽  
Zi Yae Kang ◽  
Xiaolun Sun ◽  
Pon Velayutham Anandh Babu ◽  
Dongmin Liu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Animal Study ◽  
Natural Compound ◽  
Nuclear Translocation ◽  
Protective Effects ◽  
Monocyte Adhesion ◽  
Tnf Α

Resveratrol, a natural compound in grapes and red wine, has drawn attention due to potential cardiovascular-related health benefits. However, its effect on vascular inflammation at physiologically achievable concentrations is largely unknown. In this study, resveratrol in concentrations as low as 1 μm suppressed TNF-α-induced monocyte adhesion to human EA.hy926 endothelial cells (ECs), a key event in the initiation and development of atherosclerosis. Low concentrations of resveratrol (0.25–2 μm) also significantly attenuated TNF-α-stimulated mRNA expressions of MCP-1/CCL2 and ICAM-1, which are vital mediators of EC-monocyte adhesion molecules and cytokines for cardiovascular plaque formation. Additionally, resveratrol diminished TNF-α-induced IκB-α degradation and subsequent nuclear translocation of NF-κB p65 in ECs. In the animal study, resveratrol supplementation in diet significantly diminished TNF-α-induced increases in circulating levels of adhesion molecules and cytokines, monocyte adhesion to mouse aortic ECs, F4/80-positive macrophages and VCAM-1 expression in mice aortas and restored the disruption in aortic elastin fiber caused by TNF-α treatment. The animal study also confirmed that resveratrol blocks the activation of NF-κB In Vivo. In conclusion, resveratrol at physiologically achievable concentrations displayed protective effects against TNF-α-induced vascular endothelial inflammation in vitro and In Vivo. The ability of resveratrol in reducing inflammation may be associated with its role as a down-regulator of the NF-κB pathway.

scholarly journals Leukocyte-endothelial adhesion molecules

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2068-2101 ◽  
Author(s):  
TM Carlos ◽  
JM Harlan
Keyword(s):  
Adhesion Molecules ◽  
Sufficient Information ◽  
Leukocyte Integrins ◽  
Endothelial Adhesion Molecules ◽  
And Migration ◽  
Definition Of ◽  
The Individual ◽  
Exciting Area

In the 9 years since the last review on leukocyte and endothelial interactions was published in this journal many of the critical structures involved in leukocyte adherence to and migration across endothelium have been elucidated. With the advent of cell and molecular biology approaches, investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of “anti-adhesion” therapy in humans. The molecular cloning and definition of the adhesive functions of the leukocyte integrins, endothelial members of the Ig gene superfamily, and the selectins has already provided sufficient information to construct an operative paradigm of the molecular basis of leukocyte emigration. The regulation of these adhesion molecules by chemoattractants, cytokines, or chemokines, and the interrelationships of adhesion pathways need to be examined in vitro and, particularly, in vivo. Additional studies are required to dissect the contribution of the individual adhesion molecules to leukocyte emigration in various models of inflammation or immune reaction. Certainly, new adhesion structures will be identified, and the current paradigm of leukocyte emigration will be refined. The promise of new insights into the biology and pathology of the inflammatory and immune response, and the potential for new therapies for a wide variety of diseases assures that this will continue to be an exciting area of investigation.

scholarly journals Novel Vascular Molecule Involved in Monocyte Adhesion to Aortic Endothelium in Models of Atherogenesis

1997 ◽  
Vol 185 (12) ◽  
pp. 2069-2077 ◽  
Author(s):  
Leslie M. McEvoy ◽  
Hailing Sun ◽  
Philip S. Tsao ◽  
John P. Cooke ◽  
Judith A. Berliner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ex Vivo ◽  
Critical Role ◽  
Constitutive Expression ◽  
Monocyte Adhesion ◽  
Aortic Endothelial Cells ◽  
Aortic Endothelium ◽  
Aortic Endothelial

Adhesion of monocytes to the endothelium in lesion-prone areas is one of the earliest events in fatty streak formation leading to atherogenesis. The molecular basis of increased monocyte adhesion is not fully characterized. We have identified a novel vascular monocyte adhesion-associated protein, VMAP-1, that plays a role in adhesion of monocytes to activated endothelium. Originally selected for its ability to block binding of a mouse monocyte-like cell line (WEHI78/24) to cytokine- or LPS-stimulated cultured mouse endothelial cells in vitro, antiVMAP-1 mAb LM151 cross-reacts with rabbit endothelium and blocks binding of human monocytes to cultured rabbit aortic endothelial cells stimulated with minimally modified low density lipoprotein, thought to be a physiologically relevant atherogenic stimulus. Most importantly, LM151 prevents adhesion of normal monocytes and monocytoid cells to intact aortic endothelium from cholesterol-fed rabbits in an ex vivo assay. VMAP-1 is a 50-kD protein. Immunohistology of vessels reveals focal constitutive expression in aorta and other large vessels. VMAP-1 is thus a novel vascular adhesion-associated protein that appears to play a critical role in monocyte adhesion to aortic endothelial cells in atherogenesis in vivo.

Involvement of adhesion molecules in human monocyte adhesion to and transmigration through endothelial cells in vitro

1994 ◽  
Vol 108 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Masafumi Takahashi ◽  
Uichi Ikeda ◽  
Jun-Ichi Masnama ◽  
Sei-Ichi Kitagawa ◽  
Tadashi Kasahara ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Human Monocyte ◽  
Monocyte Adhesion

scholarly journals Leukocyte-endothelial adhesion molecules

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2068-2101 ◽  
Author(s):  
TM Carlos ◽  
JM Harlan
Keyword(s):  
Adhesion Molecules ◽  
Sufficient Information ◽  
Leukocyte Integrins ◽  
Endothelial Adhesion Molecules ◽  
And Migration ◽  
Definition Of ◽  
The Individual ◽  
Exciting Area

Abstract In the 9 years since the last review on leukocyte and endothelial interactions was published in this journal many of the critical structures involved in leukocyte adherence to and migration across endothelium have been elucidated. With the advent of cell and molecular biology approaches, investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of “anti-adhesion” therapy in humans. The molecular cloning and definition of the adhesive functions of the leukocyte integrins, endothelial members of the Ig gene superfamily, and the selectins has already provided sufficient information to construct an operative paradigm of the molecular basis of leukocyte emigration. The regulation of these adhesion molecules by chemoattractants, cytokines, or chemokines, and the interrelationships of adhesion pathways need to be examined in vitro and, particularly, in vivo. Additional studies are required to dissect the contribution of the individual adhesion molecules to leukocyte emigration in various models of inflammation or immune reaction. Certainly, new adhesion structures will be identified, and the current paradigm of leukocyte emigration will be refined. The promise of new insights into the biology and pathology of the inflammatory and immune response, and the potential for new therapies for a wide variety of diseases assures that this will continue to be an exciting area of investigation.

scholarly journals Conversion of stem cells from apical papilla into endothelial cells by small molecules and growth factors

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Baicheng Yi ◽  
Tian Ding ◽  
Shan Jiang ◽  
Ting Gong ◽  
Hitesh Chopra ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Small Molecules ◽  
Adhesion Molecules ◽  
Small Molecule ◽  
Cell Type ◽  
Apical Papilla

Abstract Objectives Recently, a new strategy has been developed to directly reprogram one cell type towards another targeted cell type using small molecule compounds. Human fibroblasts have been chemically reprogrammed into neuronal cells, Schwann cells and cardiomyocyte-like cells by different small molecule combinations. This study aimed to explore whether stem cells from apical papilla (SCAP) could be reprogrammed into endothelial cells (ECs) using the same strategy. Materials and methods The expression level of endothelial-specific genes and proteins after chemical induction of SCAP was assessed by RT-PCR, western blotting, flow cytometry and immunofluorescence. The in vitro functions of SCAP-derived chemical-induced endothelial cells (SCAP-ECs) were evaluated by tube-like structure formation assay, acetylated low-density lipoprotein (ac-LDL) uptake and NO secretion detection. The proliferation and the migration ability of SCAP-ECs were evaluated by CCK-8 and Transwell assay. LPS stimulation was used to mimic the inflammatory environment in demonstrating the ability of SCAP-ECs to express adhesion molecules. The in vivo Matrigel plug angiogenesis assay was performed to assess the function of SCAP-ECs in generating vascular structures using the immune-deficient mouse model. Results SCAP-ECs expressed upregulated endothelial-specific genes and proteins; displayed endothelial transcriptional networks; exhibited the ability to form functional tubular-like structures, uptake ac-LDL and secrete NO in vitro; and contributed to generate blood vessels in vivo. The SCAP-ECs could also express adhesion molecules in the pro-inflammatory environment and have a similar migration and proliferation ability as HUVECs. Conclusions Our study demonstrates that the set of small molecules and growth factors could significantly promote endothelial transdifferentiation of SCAP, which provides a promising candidate cell source for vascular engineering and treatment of ischemic diseases.

Salusin-β accelerates inflammatory responses in vascular endothelial cells via NF-κB signaling in LDL receptor-deficient mice in vivo and HUVECs in vitro

2012 ◽  
Vol 303 (1) ◽  
pp. H96-H105 ◽  
Author(s):  
Takayuki Koya ◽  
Takuro Miyazaki ◽  
Takuya Watanabe ◽  
Masayoshi Shichiri ◽  
Takashi Atsumi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Ldl Receptor ◽  
Monocyte Adhesion ◽  
Deficient Mice

The bioactive peptide salusin-β is highly expressed in human atheromas; additionally, infusion of antiserum against salusin-β suppresses the development of atherosclerosis in atherogenic mice. This study examined the roles of salusin-β in vascular inflammation during atherogenesis. Infusion of antiserum against salusin-β attenuated the induction of VCAM-1, monocyte chemoattractant protein (MCP)-1, and IL-1β and as well as nuclear translocation of NF-κB in aortic endothelial cells (ECs) of LDL receptor-deficient mice, which led to the prevention of monocyte adhesion to aortic ECs. In vitro experiments indicated that salusin-β directly enhances the expression levels of proinflammatory molecules, including VCAM-1, MCP-1, IL-1β, and NADPH oxidase 2, as well as THP-1 monocyte adhesion to cultured human umbilical vein ECs (HUVECs). Both salusin-β-induced VCAM-1 induction and monocyte/HUVEC adhesion were suppressed by pharmacological inhibitors of NF-κB, e.g., Bay 11-7682 and curcumin. Furthermore, the VCAM-1 induction was significantly prevented by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY-294002, whereas it was accelerated by the ERK inhibitor, U-0126. Treatment of HUVECs with salusin-β, but not with salusin-α, accelerated oxidative stress and nuclear translocation of NF-κB as well as phosphorylation and degradation of IκB-α, an endogenous inhibitor of NF-κB. Thus, salusin-β enhanced monocyte adhesion to vascular ECs through NF-κB-mediated inflammatory responses in ECs, which can be modified by PI3K or ERK signals. These findings are suggestive of a novel role of salusin-β in atherogenesis.

Abstract 201: A New Multimodal Contrast Agent for Molecular Imaging of Adhesion Molecules Expressed in Atherosclerosis

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Mona Ahmed ◽  
Björn Gustafsson ◽  
Kenneth Caidahl
Keyword(s):  
Endothelial Cells ◽  
Contrast Agent ◽  
Adhesion Molecules ◽  
Laser Scanning ◽  
Specific Interaction ◽  
Negative Control ◽  
Laser Scanning Microscopy ◽  
Confocal Laser

Background: Inflammation is involved in many chronic diseases, one of which is atherosclerosis. Early detection of inflammation could improve clinical management. Most existing contrast agents on the market are non-specific and single-modal. Our aim was to apply an innovative new multimodal contrast agent, a polyvinyl alcohol based microbubble (MB), to target adhesion molecules expressed in atherosclerosis, opening a new scenario for biomedicine. Objective: To evaluate a contrast agent with different surface modifications and their adhesion to inflammatory in vitro models as a proof of concept, by imaging inflamed endothelium, that is involved in the pathogenesis of atherosclerosis. Methods: Microbubbles were antibody (Ab) or peptide conjugated to the adhesion molecule of interest. To evaluate attachment between MBs and an inflamed murine cell line, endothelial cells (EC), confocal laser scanning microscopy (CLSM) and flow cytometry (FACS) were used. To verify expression of cell adhesion molecules we used FACS and western blot. Stimulated and non-stimulated cells were incubated with MBs conjugated with active ligands, or a negative control. Results: In endothelial cells CLSM showed an increased uptake, or adherence, of peptide-conjugated microbubbles compared to non-stimulated control. MBs tagged with Abs against; ICAM-1, VCAM-1, E-Selectin, or with Cyclic Arginine-Glycine-Aspartate (cRGD) peptide showed stronger adherence to EC compared to non-targeted control. Microbubbles labeled with cRGD-peptide was shown to be the most prominent, indicating a specific interaction. Conclusions: Adhesion molecules expressed in atherosclerosis may be targeted by our labeled multimodal contrast agent in vitro , with potential for disease specific diagnostics in vivo.

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