Panax notoginseng Reduces Atherosclerotic Lesions in ApoE-Deficient Mice and Inhibits TNF-α-Induced Endothelial Adhesion Molecule Expression and Monocyte Adhesion

2009 ◽  
Vol 57 (15) ◽  
pp. 6692-6697 ◽  
Author(s):  
Jian-Bo Wan ◽  
Simon Ming-Yuen Lee ◽  
Jing-Dong Wang ◽  
Nan Wang ◽  
Cheng-Wei He ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Panax Notoginseng ◽  
Adhesion Molecule Expression ◽  
Monocyte Adhesion ◽  
Endothelial Adhesion Molecule ◽  
Atherosclerotic Lesions ◽  
Tnf Α ◽  
Deficient Mice

Vascular bed origin dictates flow pattern regulation of endothelial adhesion molecule expression

2007 ◽  
Vol 292 (5) ◽  
pp. H2167-H2175 ◽  
Author(s):  
Heiko Methe ◽  
Mercedes Balcells ◽  
Maria del Carmen Alegret ◽  
Marina Santacana ◽  
Blanca Molins ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Adhesion Molecule ◽  
Immune Cell ◽  
Adhesion Molecule Expression ◽  
Endothelial Adhesion Molecule ◽  
Vascular Bed ◽  
Pathological Conditions ◽  
Coronary Artery Flow ◽  
Tnf Α ◽  
Artery Flow

Endothelial cell phenotypes markedly differ, depending upon function and vascular bed of origin. Differences might account for specific susceptibility to pathological conditions. As leukocyte adhesion to activated endothelium is the initiating event in a range of diseases, we compared the influence of vascular bed-specific flow patterns on adhesion molecule expression in human saphenous vein (HSVEC) and coronary artery endothelial cells (HCAEC). In vitro, immune cell attachment was increased 1.6-fold when tumor necrosis factor (TNF)-α-stimulated HSVEC were exposed to coronary artery flow in place of physiological venous flow and 1.9-fold higher compared with attachment to cytokine-stimulated HCAEC exposed to coronary artery flow. This was associated with increased concentrations of soluble E-selectin, VCAM-1, and ICAM-1 in supernatants of HSVEC exposed to coronary artery flow compared with HCAEC exposed to the same flow pattern. Venous and coronary artery flow both increased TNF-α-induced E-selectin and ICAM-1 expression on HSVEC, but only coronary artery flow increased VCAM-1 expression. In marked contrast to HSVEC, venous and coronary artery flow attenuated TNF-α-induced E-selectin and VCAM-1 expression on HCAEC, whereas coronary artery flow further induced ICAM-1 on cytokine-stimulated HCAEC. With the exception of cytokine-induced ICAM-1, adhesion molecule expression on HSVEC exposed to coronary artery flow exceeded expression on HCAEC. Thus ICAM-1 expression involves complex flow-dependent and -independent pathways with marked dissimilarities between the two endothelial cell types studied. Interestingly, Kruppel-like factor (KLF) 4 overexpression in HCAEC and HSVEC significantly reduced TNF-α-induced E-selectin and VCAM-1 expression in static conditions, while ICAM-1 expression remained constant. Furthermore, both flow patterns induced KLF2 and KLF4 expression in HCAEC and HSVEC. Venous and coronary artery flow differentially influence endothelial adhesion molecule and transcription factor expression, depending on the vascular bed of origin. Differences in adhesion molecule expression and subsequent immune cell adhesion between HSVEC and HCAEC may contribute to different susceptibility to pathological conditions.

Abstract 527: The Functional Significance of the Adenosine A 2b Receptor in the Internal Mammary Artery

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Stephen R Archacki ◽  
Qing K Wang
Keyword(s):  
Cell Adhesion ◽  
Coronary Arteries ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Transendothelial Migration ◽  
Adhesion Molecule Expression ◽  
Monocyte Adhesion ◽  
Knowing That ◽  
Mammary Arteries ◽  
Internal Mammary

Objective: The endothelium is the initial target that leads to cardiovascular disease. Knowing that the internal mammary arteries (IMA) are resistant to the development of atherosclerosis, which contrasts with coronary arteries (Cor) which are athero-prone, we hypothesize that genes over-expressed in the endothelial cells (ECs) of between these two arteries will identify genes that resist atherosclerosis. Methods and Results: Microarray analysis showed over 1,000 differentially expressed in the ECs of IMA vs Cor. The most statistically significant different gene was the adenosine A 2B receptor. This indicates the A 2B receptor may be involved in a resistance to atherosclerosis. Western blot analysis showed higher A 2B expression in the IMA than in coronary arteries with or without disease from proteins harvested from these human arteries and ECs. Overexpression of A 2B in ECs blunted: monocyte adhesion, cell adhesion molecule expression, migration, and the transendothelial migration of monocytes-- processes directly associated with the development of atherosclerosis. Knockdown of A 2B expression by siRNA promoted these processes. Conclusions: ECs derived from the IMA and Cor are distinctly different in gene expression, which may be responsible for their differential sensitivities for atherosclerosis. This study defined how the A 2B receptor may act as an atherosclerotic-resistance gene, which blunted monocyte adhesion and cell adhesion molecule expression, EC migration and retarded the transendothelial migration of monocytes.

scholarly journals High-mannose intercellular adhesion molecule-1 enhances CD16+ monocyte adhesion to the endothelium

2019 ◽  
Vol 317 (5) ◽  
pp. H1028-H1038 ◽  
Author(s):  
Kellie Regal-McDonald ◽  
Brittney Xu ◽  
Jarrod W. Barnes ◽  
Rakesh P. Patel
Keyword(s):  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Proximity Ligation Assay ◽  
Dependent Manner ◽  
Monocyte Adhesion ◽  
Monocyte Subsets ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α ◽  
High Mannose

Human monocytes have been classified into three distinct groups, classical (anti-inflammatory; CD14+/CD16−), nonclassical (patrolling; CD14+/CD16++), and intermediate (proinflammatory; CD14++/CD16+). Adhesion of nonclassical/intermediate monocytes with the endothelium is important for innate immunity, and also vascular inflammatory disease. However, there is an incomplete understanding of the mechanisms that regulate CD16+ versus CD16− monocyte adhesion to the inflamed endothelium. Here, we tested the hypothesis that a high-mannose (HM) N-glycoform of intercellular adhesion molecule-1 (ICAM-1) on the endothelium mediates the selective recruitment of CD16+ monocytes. Using TNF-α treatment of human umbilical vein endothelial cells (HUVECs), and using proximity ligation assay for detecting proximity of specific N-glycans and ICAM-1, we show that TNF-α induces HM-ICAM-1 formation on the endothelial surface in a time-dependent manner. We next measured CD16− or CD16+ monocyte rolling and adhesion to TNF-α-treated HUVECs in which HM- or hybrid ICAM-1 N-glycoforms were generated using the α-mannosidase class I and II inhibitors, kifunensine and swainsonine, respectively. Expression of HM-ICAM-1 selectively enhanced CD16+ monocyte adhesion under flow with no effect on CD16− monocytes noted. CD16+ monocyte adhesion was abrogated by blocking either HM epitopes or ICAM-1. A critical role for HM-ICAM-1 in mediating CD16+ monocyte rolling and adhesion was confirmed using COS-1 cells engineered to express HM or complex ICAM-1 N-glycoforms. These data suggest that HM-ICAM-1 selectively recruits nonclassical/intermediate CD16+ monocytes to the activated endothelium. NEW & NOTEWORTHY Monocyte subsets have been associated with cardiovascular disease, yet it is unknown how different subsets are recruited to the endothelium. This study demonstrates the formation of distinct ICAM-1 N-glycoforms in the activated endothelium and reveals a key role for high mannose ICAM-1 in mediating proinflammatory CD16+ monocyte adhesion. Presented data identify roles for endothelial N-glycans in recruiting specific monocyte subsets during inflammation.

scholarly journals Corylin Inhibits Vascular Cell Inflammation, Proliferation and Migration and Reduces Atherosclerosis in ApoE-Deficient Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 275
Author(s):  
Chin-Chuan Chen ◽  
Hung-Yuan Li ◽  
Yann-Lii Leu ◽  
Yu-Ju Chen ◽  
Chia-Jen Wang ◽  
...  
Keyword(s):  
Flavonoid Compound ◽  
Ros Production ◽  
Monocyte Adhesion ◽  
Vascular Cell ◽  
Vsmc Proliferation ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
And Migration ◽  
Deficient Mice ◽  
Proliferation And Migration

Atherosclerosis is a complex disease that includes several events, including reactive oxygen species (ROS) stress, inflammation, endothelial dysfunction, lipid deposition, and vascular smooth muscle cell (VSMC) proliferation and migration, which result in atherosclerotic plaque formation. Corylin, a flavonoid compound, is known to exhibit antioxidative, anti-inflammatory and antiproliferative effects. However, it remains unknown whether corylin could modulate atherogenesis. Here, we identified the anti-inflammatory effect of corylin in tumor necrosis factor-α (TNF-α)-induced vascular cells. In human umbilical vein endothelial cells (HUVECs), corylin suppressed TNF-α-induced monocyte adhesion to the HUVECs and transmigration by downregulating the ROS/JNK/nuclear factor-kappa beta (NF-κB) p65 pathway. In VSMCs, corylin inhibited TNF-α-induced monocyte adhesion by suppressing ROS production, mitogen-activated protein kinase (MAPK) phosphorylation and NF-κB p65 translocation. In platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs, corylin inhibited PDGF-BB-induced VSMC proliferation and migration through regulating the mammalian target of rapamycin (mTOR)/dynamin-1-like protein 1 (Drp1) signaling cascade. In addition, corylin treatment not only attenuated atherosclerotic lesions, ROS production, vascular cell adhesion protein-1 (VCAM-1) expression, monocyte adhesion and VSMC proliferation in apolipoprotein E (ApoE)-deficient mice but also inhibited neointimal hyperplasia in endothelial-denuded mice. Thus, corylin may be a potential prevention and treatment for atherosclerosis.

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