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Journal articles on the topic 'Vascular cell adhesion molecule'

Author: Grafiati

Published: 28 May 2022

Last updated: 18 July 2025

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1

Fotis, Lampros, Dionysios Giannakopoulos, Lela Stamogiannou, and Maria Xatzipsalti. "Intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 in children. Do they play a role in the progression of atherosclerosis?" HORMONES 11, no. 2 (2012): 140–46. http://dx.doi.org/10.14310/horm.2002.1340.

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Yoshida, Norimasa, Kyoichi Kassai, Hironobu Murase, et al. "Effects ofHelicobacter pyloriWater Extract on Expression of Endothelial Adhesion Molecules." Canadian Journal of Gastroenterology 18, no. 6 (2004): 387–91. http://dx.doi.org/10.1155/2004/158638.

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The present study investigated whetherHelicobacter pyloriwater extract induces the upregulation of intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin on human umbilical vein endothelial cells, using an ELISA. The nature of the substances mediating this upregulation was also analyzed.H pyloriwater extract derived from type strain (NCTC 11637) significantly upregulated intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin to the same extent as interleukin-1. Treatments with extracts from clinical strains showed no significant increas

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Raynor, B. Denise, and Sampath Parthasarathy. "Vascular cell adhesion molecule in pregnancy." American Journal of Obstetrics and Gynecology 179, no. 1 (1998): 279. http://dx.doi.org/10.1016/s0002-9378(98)70303-5.

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4

Wuthrich, R. P. "Intercellular adhesion molecules and vascular cell adhesion molecule-1 and the kidney." Journal of the American Society of Nephrology 3, no. 6 (1992): 1201–11. http://dx.doi.org/10.1681/asn.v361201.

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Adhesion molecules such as intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 are expressed in the kidney and are regulated by proinflammatory cytokines. These adhesion molecules play an important role in the binding and activation process of leukocytes and are of importance in inflammatory kidney diseases. This review article describes current knowledge regarding the structure, expression, and functional role of adhesion molecules and their significance in immune-mediated renal diseases.

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Hajialilo, M., P. Tayari, A. Ghorbanihaghjo, A. Khabbazi, A. Malek Mahdavi, and N. Rashtchizadeh. "Relationship between serum vascular cell adhesion molecule-1 and endothelin-1 levels with organ involvement and disease activity in systemic lupus erythematosus patients." Lupus 27, no. 12 (2018): 1918–25. http://dx.doi.org/10.1177/0961203318796285.

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Background Endothelial dysfunction plays an important role in pathogenesis of systemic lupus erythematosus (SLE). Considering the importance of serum soluble vascular cell adhesion molecule-1 as the most abundant of the circulating adhesion molecules increased as a result of endothelial dysfunction and the role of endothelin-1 in pathophysiology of SLE, this study aimed to evaluate serum soluble vascular cell adhesion molecule-1 and endothelin-1 levels in SLE patients compared to healthy subjects. Methods In this cross-sectional study, 60 SLE patients according to the Systemic Lupus Internatio

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Park, Sunyoung, Christine M. Sorenson, and Nader Sheibani. "PECAM-1 isoforms, eNOS and endoglin axis in regulation of angiogenesis." Clinical Science 129, no. 3 (2015): 217–34. http://dx.doi.org/10.1042/cs20140714.

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Vascular development and maintenance of proper vascular function through various regulatory mechanisms are critical to our wellbeing. Delineation of the regulatory processes involved in development of the vascular system and its function is one of the most important topics in human physiology and pathophysiology. Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31), a cell adhesion molecule with proangiogenic and proinflammatory activity, has been the subject of numerous studies. In the present review, we look at the important roles that PECAM-1 and its isoforms play during angiogenesi

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Tong, Ming, Yu Jiang, Da Xia, et al. "Elevated Expression of Serum Endothelial Cell Adhesion Molecules in COVID-19 Patients." Journal of Infectious Diseases 222, no. 6 (2020): 894–98. http://dx.doi.org/10.1093/infdis/jiaa349.

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Abstract In a retrospective study of 39 COVID-19 patients and 32 control participants in China, we collected clinical data and examined the expression of endothelial cell adhesion molecules by enzyme-linked immunosorbent assays. Serum levels of fractalkine, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular adhesion protein-1 (VAP-1) were elevated in patients with mild disease, dramatically elevated in severe cases, and decreased in the convalescence phase. We conclude the increased expression of endothelial cell adhesion molecules is related t

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Storer, Kingsley P., Jian Tu, Marcus A. Stoodley, and Robert I. Smee. "Expression of Endothelial Adhesion Molecules After Radiosurgery in an Animal Model of Arteriovenous Malformation." Neurosurgery 67, no. 4 (2010): 976–83. http://dx.doi.org/10.1227/neu.0b013e3181ee36bc.

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Abstract BACKGROUND: Endothelial adhesion molecules may be important in the response of brain arteriovenous malformations (AVMs) to radiosurgery. In addition to a putative role in the occlusive process after radiosurgery, they may serve as potential targets for biological strategies to accelerate intravascular thrombosis. OBJECTIVE: To determine the temporal expression of E-selectin and vascular cell adhesion molecule-1 in an animal model of AVMs. METHODS: Forty-one Sprague-Dawley rats underwent surgical creation of a carotid-to-jugular anastomosis. Radiosurgery (25 Gy) was delivered to the mo

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Langley, Robert R., Janice Russell, Michael J. Eppihimer, et al. "Quantification of murine endothelial cell adhesion molecules in solid tumors." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 3 (1999): H1156—H1166. http://dx.doi.org/10.1152/ajpheart.1999.277.3.h1156.

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Coordinated adhesive interactions between lymphocyte receptors and endothelial cell adhesion molecules (CAMs) are a prerequisite for effector cell entry into tumor stroma. Whereas the diminished leukocyte-endothelial cell interactions observed in tumor microvessels have been attributed to a reduced expression of endothelial CAMs, there is no quantitative data bearing on this issue. The dual-radiolabeled monoclonal antibody technique was used to quantify constitutive and tumor necrosis factor (TNF)-α-induced expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecu

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Lee, Tae Hoon. "Lactoferrin inhibits immune cell adhesion via suppression of cell adhesion molecules expression in hypoxia/reoxygenation animal model." Journal of Immunology 200, no. 1_Supplement (2018): 42.10. http://dx.doi.org/10.4049/jimmunol.200.supp.42.10.

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Abstract Lactoferrin (Lf), an 80 kDa iron binding protein, belongs to transferrin family found in secretions such as milk and in plasma secreted from neutrophils granules upon inflammatory stimulation. Lf is a multifunctional protein mainly involved in both the innate and adaptive immune defenses. In this study, we investigated the anti-adherent activity of Lf in hypoxia/reoxygenation (H/R)-stimulated human endothelial cells (HUVECs). Lf dramatically reduced the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) by hypoxia-situation HUVECs.

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Shieh, Chi-Chang, Bhanu K. Sadasivan, Gary J. Russell, Michael P. Schön, Christina M. Parker, and Michael B. Brenner. "Lymphocyte Adhesion to Epithelia and Endothelia Mediated by the Lymphocyte Endothelial-Epithelial Cell Adhesion Molecule Glycoprotein." Journal of Immunology 163, no. 3 (1999): 1592–601. http://dx.doi.org/10.4049/jimmunol.163.3.1592.

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Abstract Upon encountering the relevant vascular bed, lymphocytes attach to endothelial adhesion molecules, transmigrate out of circulation, and localize within tissues. Lymphocytes may then be retained at microanatomic sites, as in tissues, or they may continue to migrate to the lymphatics and recirculate in the blood. Lymphocytes also interact transiently, but with high avidity, with target cells or APC that are infected with microbes or have taken up exogenous foreign Ags. This array of adhesive capabilities is mediated by the selective expression of lymphocyte adhesion molecules. Here, we

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Ley, Klaus, and Hong Zhang. "Dances with leukocytes: how tetraspanin-enriched microdomains assemble to form endothelial adhesive platforms." Journal of Cell Biology 183, no. 3 (2008): 375–76. http://dx.doi.org/10.1083/jcb.200809173.

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Rather than just providing an unstructured adhesive surface for leukocytes, cytokine-activated endothelial cells assemble preexisting tetraspanin-enriched microdomains to form endothelial adhesive platforms (EAPs) and endothelial docking structures. In this issue of the Journal of Cell Biology, Barreiro et al. (Barreiro, O., M. Zamai, M. Yáñez-Mó, E. Tejera, P. López-Romero, P.N. Monk, E. Gratton, V.R. Caiolfa, and F. Sánchez-Madrid. 2008. J. Cell Biol. 183:527–542) show how the immunoglobulin superfamily adhesion molecules intercellular adhesion molecule (ICAM)–1 and vascular cell adhesi

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Ho, May, and Nicholas J. White. "Molecular mechanisms of cytoadherence in malaria." American Journal of Physiology-Cell Physiology 276, no. 6 (1999): C1231—C1242. http://dx.doi.org/10.1152/ajpcell.1999.276.6.c1231.

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Microbial pathogens subvert host adhesion molecules to disseminate or to enter host cells to promote their own survival. One such subversion is the cytoadherence of Plasmodium falciparum-infected erythrocytes (IRBC) to vascular endothelium, which protects the parasite from being removed by the spleen. The process results in microcirculatory obstruction and subsequent hypoxia, metabolic disturbances, and multiorgan failure, which are detrimental to the host. Understanding the molecular events involved in these adhesive interactions is therefore critical both in terms of pathogenesis and implica

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Hordijk, P. L., E. Anthony, F. P. Mul, R. Rientsma, L. C. Oomen, and D. Roos. "Vascular-endothelial-cadherin modulates endothelial monolayer permeability." Journal of Cell Science 112, no. 12 (1999): 1915–23. http://dx.doi.org/10.1242/jcs.112.12.1915.

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Vascular endothelial (VE)-cadherin is the endothelium-specific member of the cadherin family of homotypic cell adhesion molecules. VE-cadherin, but not the cell adhesion molecule platelet/endothelial cell adhesion molecule (PECAM-1), markedly colocalizes with actin stress fibers at cell-cell junctions between human umbilical vein endothelial cells. Inhibition of VE-cadherin-mediated, but not PECAM-1-mediated, adhesion induced reorganization of the actin cytoskeleton, loss of junctional VE-cadherin staining and loss of cell-cell adhesion. In functional assays, inhibition of VE-cadherin caused i

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15

Elangbam, C. S., C. W. Qualls, and R. R. Dahlgren. "Cell Adhesion Molecules—Update." Veterinary Pathology 34, no. 1 (1997): 61–73. http://dx.doi.org/10.1177/030098589703400113.

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Cell adhesion molecules are glycoproteins expressed on the cell surface and play an important role in inflammatory as well as neoplastic diseases. There are four main groups: the integrin family, the immunoglobulin superfamily, selectins, and cadherins. The integrin family has eight subfamilies, designated as β1, through β8. The most widely studied subfamilies are β1 (CD29, very late activation [VLA] members), β2 (leukocyte integrins such as CDlla/CD18, CDllb/CD18, CDllc/CD18, and αdβ2), β3 (CD61, eytoadhesions), and β7 (α4β7 and αEβ7). The immunoglobulin superfamily includes leukocyte functio

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Shimonaka, Mika, Koko Katagiri, Toshinori Nakayama, et al. "Rap1 translates chemokine signals to integrin activation, cell polarization, and motility across vascular endothelium under flow." Journal of Cell Biology 161, no. 2 (2003): 417–27. http://dx.doi.org/10.1083/jcb.200301133.

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Chemokines arrest circulating lymphocytes within the vasculature through the rapid up-regulation of leukocyte integrin adhesive activity, promoting subsequent lymphocyte transmigration. However, the key regulatory molecules regulating this process have remained elusive. Here, we demonstrate that Rap1 plays a pivotal role in chemokine-induced integrin activation and migration. Rap1 was activated by secondary lymphoid tissue chemokine (SLC; CCL21) and stromal-derived factor 1 (CXCL4) treatment in lymphocytes within seconds. Inhibition of Rap1 by Spa1, a Rap1-specific GTPase-activating protein, a

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Pierce, J. W., M. A. Read, H. Ding, F. W. Luscinskas, and T. Collins. "Salicylates inhibit I kappa B-alpha phosphorylation, endothelial-leukocyte adhesion molecule expression, and neutrophil transmigration." Journal of Immunology 156, no. 10 (1996): 3961–69. http://dx.doi.org/10.4049/jimmunol.156.10.3961.

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Abstract The expression of leukocyte adhesion molecules on endothelial cells is induced by TNF-alpha and other inflammatory cytokines. This induction of endothelial-leukocyte adhesion molecule-1, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 requires the transcription factor nuclear factor-kappa B (NF-kappa B). Recent work has suggested that some nonsteroidal anti-inflammatory agents, including sodium salicylate and aspirin, can inhibit NF-kappa B-dependent gene activation. We studied the effects of salicylates on expression of adhesion molecules in HUVECs. We found

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Albelda, S. M., P. D. Oliver, L. H. Romer, and C. A. Buck. "EndoCAM: a novel endothelial cell-cell adhesion molecule." Journal of Cell Biology 110, no. 4 (1990): 1227–37. http://dx.doi.org/10.1083/jcb.110.4.1227.

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Cell-cell adhesion is controlled by many molecules found on the cell surface. In addition to the constituents of well-defined junctional structures, there are the molecules that are thought to play a role in the initial interactions of cells and that appear at precise times during development. These include the cadherins and cell adhesion molecules (CAMs). Representatives of these families of adhesion molecules have been isolated from most of the major tissues. The notable exception is the vascular endothelium. Here we report the identification of a cell surface molecule designated "endoCAM" (

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Ockenhouse, C. F., T. Tegoshi, Y. Maeno, et al. "Human vascular endothelial cell adhesion receptors for Plasmodium falciparum-infected erythrocytes: roles for endothelial leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1." Journal of Experimental Medicine 176, no. 4 (1992): 1183–89. http://dx.doi.org/10.1084/jem.176.4.1183.

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The clinical complications associated with severe and cerebral malaria occur as a result of the intravascular mechanical obstruction of erythrocytes infected with the asexual stages of the parasite, Plasmodium falciparum. We now report that a primary P. falciparum-infected erythrocyte (parasitized red blood cell [PRBC]) isolate from a patient with severe complicated malaria binds to cytokine-induced human vascular endothelial cells, and that this adhesion is in part mediated by endothelial leukocyte adhesion molecule 1 (ELAM-1) and vascular cell adhesion molecule 1 (VCAM-1). PRBC binding to tu

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Brandsma, Dieta, Jaap C. Reijneveld, Martin J. B. Taphoorn, et al. "Vascular Cell Adhesion Molecule-1 Is a Key Adhesion Molecule in Melanoma Cell Adhesion to the Leptomeninges." Laboratory Investigation 82, no. 11 (2002): 1493–502. http://dx.doi.org/10.1097/01.lab.0000036876.08970.c1.

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Yun, Peter L. W., Arthur A. DeCarlo, and Neil Hunter. "Gingipains of Porphyromonas gingivalis Modulate Leukocyte Adhesion Molecule Expression Induced in Human Endothelial Cells by Ligation of CD99." Infection and Immunity 74, no. 3 (2006): 1661–72. http://dx.doi.org/10.1128/iai.74.3.1661-1672.2006.

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ABSTRACT Porphyromonas gingivalis has been implicated as a key etiologic agent in the pathogenesis of destructive chronic periodontitis. Among virulence factors of this organism are cysteine proteinases, or gingipains, that have the capacity to modulate host inflammatory defenses. Intercellular adhesion molecule expression by vascular endothelium represents a crucial process for leukocyte transendothelial migration into inflamed tissue. Ligation of CD99 on endothelial cells was shown to induce expression of endothelial leukocyte adhesion molecule 1, vascular cell adhesion molecule 1, intercell

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Garrido-Urbani, Sarah, Paul F. Bradfield, Boris P. L. Lee, and Beat A. Imhof. "Vascular and epithelial junctions: a barrier for leucocyte migration." Biochemical Society Transactions 36, no. 2 (2008): 203–11. http://dx.doi.org/10.1042/bst0360203.

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Rapid mobilization of leucocytes through endothelial and epithelial barriers is key in immune system reactivity. The underlying mechanisms that regulate these processes have been the basis for many recent studies. Traditionally, leucocyte extravasation had been believed to occur through a paracellular route, which involves localized disruption of endothelial cell junctions. However, more recently, a transcellular route has been described involving the passage through the endothelial cell body. Leucocytes are also able to migrate through epithelium to monitor mucosal tissues and microenvironmen

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Hausmann, G., JM Mascaró Jr, C. Herrero, MC Cid, J. Palou, and JM Mascaró. "Cell adhesion molecule expression in cutaneous lesions of dermatomyositis." Acta Dermato-Venereologica 76, no. 3 (1996): 222–25. http://dx.doi.org/10.2340/0001555576222225.

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Chronic inflammation seems to play a major role in skin and muscle cell damage in dermatomyositis. Adhesion molecules and their ligands are fundamental in regulating inflammation. We have carried out an immunohistochemical analysis of different activation-inducible adhesion markers in 15 biopsy specimens from dermatomyositis skin lesions. Consistent findings were the increased expression of intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, inflammatory cells and focally grouped keratinocytes in contact with subepidermal inflammatory infiltrates. Immunoreactivity for vascular cel

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Weber, Nina C., Jennis Kandler, Wolfgang Schlack, Yvonne Grueber, Jan Fräßdorf та Benedikt Preckel. "Intermitted Pharmacologic Pretreatment by Xenon, Isoflurane, Nitrous Oxide, and the Opioid Morphine Prevents Tumor Necrosis Factor α–induced Adhesion Molecule Expression in Human Umbilical Vein Endothelial Cells". Anesthesiology 108, № 2 (2008): 199–207. http://dx.doi.org/10.1097/01.anes.0000299441.32091.ed.

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Background The barrier properties of the endothelium are of critical importance during pathophysiologic processes. These barrier properties depend on an intact cytoskeleton and are regulated by cell adhesion molecules. Tumor necrosis factor alpha (TNF-alpha) is known to induce cell adhesion molecule expression. In myocardium, the protective effect by xenon and isoflurane preconditioning was found to be linked to the cytoskeleton. The authors investigated the impact of different anesthetics and morphine on TNF-alpha-induced endothelial cell adhesion molecule expression. Methods Human umbilical

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Chinthamani, Sreedevi, Olutayo Odusanwo, Nandini Mondal, Joel Nelson, Sriram Neelamegham, and Olga J. Baker. "Lipoxin A4inhibits immune cell binding to salivary epithelium and vascular endothelium." American Journal of Physiology-Cell Physiology 302, no. 7 (2012): C968—C978. http://dx.doi.org/10.1152/ajpcell.00259.2011.

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Lipoxins are formed by leukocytes during cell-cell interactions with epithelial or endothelial cells. Native lipoxin A4(LXA4) binds to the G protein-coupled lipoxin receptors formyl peptide receptor 2 (FPR2)/ALX and CysLT1. Furthermore, LXA4inhibits recruitment of neutrophils, by attenuating chemotaxis, adhesion, and transmigration across vascular endothelial cells. LXA4thus appears to serve as an endogenous “stop signal” for immune cell-mediated tissue injury (Serhan CN; Annu Rev Immunol 25: 101–137, 2007). The role of LXA4has not been addressed in salivary epithelium, and little is known abo

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Jeon, Hyejin, Daehyeop Lee, Joo-Yun Kim, Jae-Jung Shim, and Jae-Hwan Lee. "Limosilactobacillus reuteri HY7503 and Its Cellular Proteins Alleviate Endothelial Dysfunction by Increasing Nitric Oxide Production and Regulating Cell Adhesion Molecule Levels." International Journal of Molecular Sciences 25, no. 20 (2024): 11326. http://dx.doi.org/10.3390/ijms252011326.

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Endothelial dysfunction, which is marked by a reduction in nitric oxide (NO) production or an imbalance in relaxing and contracting factor levels, exacerbates atherosclerosis by promoting the production of cell adhesion molecules and cytokines. This study aimed to investigate the effects of Limosilactobacillus reuteri HY7503, a novel probiotic isolated from raw milk, on endothelial dysfunction. Five lactic acid bacterial strains were screened for their antioxidant, anti-inflammatory, and endothelium-protective properties; L. reuteri HY7503 had the most potent effect. In a mouse model of angiot

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DeLisser, Horace M., H. Scott Baldwin, and Steven M. Albelda. "Platelet Endothelial Cell Adhesion Molecule 1 (PECAM-1/CD31): A Multifunctional Vascular Cell Adhesion Molecule." Trends in Cardiovascular Medicine 7, no. 6 (1997): 203–10. http://dx.doi.org/10.1016/s1050-1738(97)00049-2.

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Ivanov, Danila, Maria Philippova, Vsevolod Tkachuk, Paul Erne, and Thérèse Resink. "Cell adhesion molecule T-cadherin regulates vascular cell adhesion, phenotype and motility." Experimental Cell Research 293, no. 2 (2004): 207–18. http://dx.doi.org/10.1016/j.yexcr.2003.09.030.

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Thomas, Alan J., Christopher Morris, Sue Davis, Elizabeth Jackson, Richard Harrison, and John T. O'Brien. "Soluble cell adhesion molecules in late-life depression." International Psychogeriatrics 19, no. 5 (2007): 914–20. http://dx.doi.org/10.1017/s1041610206004728.

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Background: Late-life depression has been associated with vascular diseases and with increases in circulating cytokines and cell adhesion molecules in the prefrontal cortex. We hypothesized that soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) would be increased in late-life major depression.Methods: Serum levels of sICAM-1 and sVCAM-1 were measured in subjects over 60 with major depression (N = 23), subsyndromal depression (N = 20) and controls (N = 25). Depression severity was assessed using the Montgomery-Åsberg (MDRS) and Geriatric

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Liang, Shile, and Cheng Dong. "Integrin VLA-4 enhances sialyl-Lewisx/a-negative melanoma adhesion to and extravasation through the endothelium under low flow conditions." American Journal of Physiology-Cell Physiology 295, no. 3 (2008): C701—C707. http://dx.doi.org/10.1152/ajpcell.00245.2008.

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During their passage through the circulatory system, tumor cells undergo extensive interactions with various host cells including endothelial cells. The capacity of tumor cells to form metastasis is related to their ability to interact with and extravasate through endothelial cell layers, which involves multiple adhesive interactions between tumor cells and endothelium (EC). Thus it is essential to identify the adhesive receptors on the endothelial and melanoma surface that mediate those specific adhesive interactions. P-selectin and E-selectin have been reported as adhesion molecules that med

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Sciacca, F. L., M. Stürzl, F. Bussolino, et al. "Expression of adhesion molecules, platelet-activating factor, and chemokines by Kaposi's sarcoma cells." Journal of Immunology 153, no. 10 (1994): 4816–25. http://dx.doi.org/10.4049/jimmunol.153.10.4816.

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Abstract The present study was designed to investigate whether cells cultured from Kaposi's sarcoma (KS), a vascular tumor with a prominent leukocyte infiltration, express molecules important for the recruitment and activation of leukocytes. KS cells expressed intercellular adhesion molecule-1, which was augmented by exposure to IL-1 beta or TNF-alpha. Unlike endothelial cells, resting or cytokine-activated KS cells did not express appreciable levels of intercellular adhesion molecule-2, vascular cell adhesion molecule-1, and E-selectin on their surface. Weak expression of vascular cell adhesi

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Shiu, Yan-Ting, Mark M. Udden, and Larry V. McIntire. "Perfusion with sickle erythrocytes up-regulates ICAM-1 andVCAM-1 gene expression in cultured human endothelial cells." Blood 95, no. 10 (2000): 3232–41. http://dx.doi.org/10.1182/blood.v95.10.3232.

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Abstract Sickle cell anemia is characterized by periodic vasoocclusive crises. Increased adhesion of sickle erythrocytes to vascular endothelium is a possible contributing factor to vasoocclusion. This study determined the effect of sickle erythrocyte perfusion at a venous shear stress level (1 dyne/cm2) on endothelial cell (EC) monolayers. Sickle erythrocytes up-regulated intercellular adhesion molecule-1 (ICAM-1) gene expression in cultured human endothelial cells. This was accompanied by increased cell surface expression of ICAM-1 and also elevated release of soluble ICAM-1 molecules. Expre

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Shiu, Yan-Ting, Mark M. Udden, and Larry V. McIntire. "Perfusion with sickle erythrocytes up-regulates ICAM-1 andVCAM-1 gene expression in cultured human endothelial cells." Blood 95, no. 10 (2000): 3232–41. http://dx.doi.org/10.1182/blood.v95.10.3232.010k16_3232_3241.

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Sickle cell anemia is characterized by periodic vasoocclusive crises. Increased adhesion of sickle erythrocytes to vascular endothelium is a possible contributing factor to vasoocclusion. This study determined the effect of sickle erythrocyte perfusion at a venous shear stress level (1 dyne/cm2) on endothelial cell (EC) monolayers. Sickle erythrocytes up-regulated intercellular adhesion molecule-1 (ICAM-1) gene expression in cultured human endothelial cells. This was accompanied by increased cell surface expression of ICAM-1 and also elevated release of soluble ICAM-1 molecules. Expression of

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Maple, C., G. Kirk, M. McLaren, D. Veale, and J. J. F. Belch. "A Circadian Variation Exists for Soluble Levels of Intercellular Adhesion Molecule-I and E-Selectin in Healthy Volunteers." Clinical Science 94, no. 5 (1998): 537–40. http://dx.doi.org/10.1042/cs0940537.

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1. We have previously shown a circadian variation in leucocyte activation and endothelial function which may explain why some inflammatory and vascular diseases show a circadian variation in disease activity/occurrence. 2. We have investigated the circadian variation of two soluble cell adhesion molecules, intercellular adhesion molecule-1 and E-selectin, in 10 healthy volunteers. Soluble intercellular adhesion molecule-1 is released from both activated leucocytes and endothelial cells while soluble E-selectin is released only from activated endothelium. 3. Results show a circadian variation e

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Vallely, Michael P., Paul G. Bannon, Clifford F. Hughes, and Leonard Kritharides. "Endothelial expression of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 is suppressed by postbypass plasma containing increased soluble intercellular adhesion molecule 1 and vascular cell adhesion molecule 1." Journal of Thoracic and Cardiovascular Surgery 124, no. 4 (2002): 758–67. http://dx.doi.org/10.1067/mtc.2002.123133.

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Haraldsen, G., D. Kvale, B. Lien, I. N. Farstad, and P. Brandtzaeg. "Cytokine-regulated expression of E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in human microvascular endothelial cells." Journal of Immunology 156, no. 7 (1996): 2558–65. http://dx.doi.org/10.4049/jimmunol.156.7.2558.

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Abstract Endothelial cells (EC) recruit circulating leukocytes to sites of inflammation, partly by expression of endothelial-leukocyte adhesion molecules. Whereas the regulation of some adhesion molecules is well characterized in cultured HUVEC, similar data for microvascular human test systems are limited. We studied the cytokine-regulated expression of vascular cell adhesion molecules E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in cultured human intestinal microvascular endothelial cells (HIMEC). E-selectin and VCAM-1 were induced, a

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Beckmann, Ilse, and Henk C. S. Wallenburg. "Reply to: Vascular cell adhesion molecule in pregnancy." American Journal of Obstetrics and Gynecology 179, no. 1 (1998): 279. http://dx.doi.org/10.1016/s0002-9378(98)70304-7.

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Schreiner, Erwin P., Berndt Oberhauser, and Carolyn A. Foster. "Inhibitors of vascular cell adhesion molecule-1 expression." Expert Opinion on Therapeutic Patents 13, no. 2 (2003): 149–66. http://dx.doi.org/10.1517/13543776.13.2.149.

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Wautier, Jean-Luc, and Marie-Paule Wautier. "Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders." International Journal of Molecular Sciences 21, no. 15 (2020): 5315. http://dx.doi.org/10.3390/ijms21155315.

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In physiology and pathophysiology the molecules involved in blood cell–blood cell and blood cell–endothelium interactions have been identified. Platelet aggregation and adhesion to the walls belonging to vessels involve glycoproteins (GP), GP llb and GP llla and the GP Ib–IX–V complex. Red blood cells (RBCs) in normal situations have little interaction with the endothelium. Abnormal adhesion of RBCs was first observed in sickle cell anemia involving vascular cell adhesion molecule (VCAM)-1, α4β1, Lu/BCAM, and intercellular adhesion molecule (ICAM)-4. More recently RBC adhesion was found to be

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Wagener, Frank A. D. T. G., Andreas Eggert, Otto C. Boerman, et al. "Heme is a potent inducer of inflammation in mice and is counteracted by heme oxygenase." Blood 98, no. 6 (2001): 1802–11. http://dx.doi.org/10.1182/blood.v98.6.1802.

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Abstract Various pathologic conditions, such as hemorrhage, hemolysis and cell injury, are characterized by the release of large amounts of heme. Recently, it was demonstrated that heme oxygenase (HO), the heme-degrading enzyme, and heme are able to modulate adhesion molecule expression in vitro. In the present study, the effects of heme and HO on inflammation in mice were analyzed by monitoring the biodistribution of radiolabeled liposomes and leukocytes in conjunction with immunohistochemistry. Small liposomes accumulate in inflamed tissues by diffusion because of locally enhanced vascular p

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Akin, Evren, John Aversa, and Allen C. Steere. "Expression of Adhesion Molecules in Synovia of Patients with Treatment-Resistant Lyme Arthritis." Infection and Immunity 69, no. 3 (2001): 1774–80. http://dx.doi.org/10.1128/iai.69.3.1774-1780.2001.

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ABSTRACT The expression of adhesion molecules in synovium in patients with Lyme arthritis is surely critical in the control of Borrelia burgdorferi infection but may also have pathologic consequences. For example, molecular mimicry between a dominant T-cell epitope ofB. burgdorferi outer surface protein A and an adhesion molecule, human lymphocyte function-associated antigen 1 (LFA-1), has been implicated in the pathogenesis of treatment-resistant Lyme arthritis. Using immunohistochemical methods, we examined synovial samples for expression of adhesion molecules in 29 patients with treatment-r

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Delia, D., MG Lampugnani, M. Resnati, et al. "CD34 expression is regulated reciprocally with adhesion molecules in vascular endothelial cells in vitro." Blood 81, no. 4 (1993): 1001–8. http://dx.doi.org/10.1182/blood.v81.4.1001.1001.

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Abstract Freshly cultured vascular endothelial cells express the CD34 antigen in a diffuse cell surface pattern with some concentration on microvilli. Expression is downregulated with proliferation in continuous culture and undetectable after nine population doublings but can be maintained by restraining cell proliferation and promoting cell contact. Expression of CD34 at the antigen and mRNA levels on early passage cells is rapidly downregulated by interleukin-1 beta (IL-1 beta), interferon-gamma (INF-gamma), and tumor necrosis factor-alpha (TNF- alpha) under conditions in which these ligands

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Delia, D., MG Lampugnani, M. Resnati, et al. "CD34 expression is regulated reciprocally with adhesion molecules in vascular endothelial cells in vitro." Blood 81, no. 4 (1993): 1001–8. http://dx.doi.org/10.1182/blood.v81.4.1001.bloodjournal8141001.

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Freshly cultured vascular endothelial cells express the CD34 antigen in a diffuse cell surface pattern with some concentration on microvilli. Expression is downregulated with proliferation in continuous culture and undetectable after nine population doublings but can be maintained by restraining cell proliferation and promoting cell contact. Expression of CD34 at the antigen and mRNA levels on early passage cells is rapidly downregulated by interleukin-1 beta (IL-1 beta), interferon-gamma (INF-gamma), and tumor necrosis factor-alpha (TNF- alpha) under conditions in which these ligands upregula

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44

Bajaj, Harpreet S., Chang Ye, Anthony J. Hanley, Mathew Sermer, Bernard Zinman, and Ravi Retnakaran. "Biomarkers of vascular injury and endothelial dysfunction after recent glucose intolerance in pregnancy." Diabetes and Vascular Disease Research 15, no. 5 (2018): 449–57. http://dx.doi.org/10.1177/1479164118779924.

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Objective: Women with gestational diabetes mellitus and milder gestational impaired glucose intolerance have elevated future risks of type 2 diabetes and cardiovascular disease. However, it is unclear whether they show postpartum evidence of vascular injury/dysfunction, an early event in the natural history of cardiovascular disease. Methods: In total, 337 women underwent a glucose challenge test and oral glucose tolerance test in pregnancy, yielding four gestational glucose tolerance groups: gestational diabetes mellitus, gestational impaired glucose intolerance, abnormal glucose challenge te

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Liu, Hongbin, Anthony E. Dear, Lotte B. Knudsen, and Richard W. Simpson. "A long-acting glucagon-like peptide-1 analogue attenuates induction of plasminogen activator inhibitor type-1 and vascular adhesion molecules." Journal of Endocrinology 201, no. 1 (2009): 59–66. http://dx.doi.org/10.1677/joe-08-0468.

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Glucagon-like peptide-1 (GLP-1) administration attenuates endothelial cell dysfunction in diabetic patients and inhibits tumour necrosis factor α (TNF)-mediated plasminogen activator inhibitor type-1 (PAI-1) induction in human vascular endothelial cells. The short half-life of GLP-1 mediated via degradation by the enzyme dipeptidyl peptidase 4 mandates the clinical use of long-acting GLP-1 analogues. The effects of a long-acting GLP-1 analogue on PAI-1 and vascular adhesion molecule expression in vascular endothelial cells are unknown. In this report, we demonstrate for the first time that the

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Lee, Yun Jung, Yong Pyo Lee, Chang Seob Seo, et al. "The Modulation of Nrf-2/HO-1 Signaling Axis by Carthamus tinctorius L. Alleviates Vascular Inflammation in Human Umbilical Vein Endothelial Cells." Plants 10, no. 12 (2021): 2795. http://dx.doi.org/10.3390/plants10122795.

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Carthamus tinctorius L., known as safflower, has been used in traditional treatment for cardiovascular, cerebrovascular, and diabetic vascular complications. We proposed to investigate how the ethanol extract of Carthamus tinctorius L. (ECT) can be used ethnopharmacologically and alleviate vascular inflammatory processes under cytokine stimulation in human vascular endothelial cells. Using the optimized HPLC method, six markers were simultaneously analyzed for quality control of ECT. Pretreatment with ECT (10–100 μg/mL) significantly reduced the increase of leukocyte adhesion to HUVEC by TNF-α

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Imhof, B. A., P. Ruiz, B. Hesse, R. Palacios, and D. Dunon. "EA-1, a novel adhesion molecule involved in the homing of progenitor T lymphocytes to the thymus." Journal of Cell Biology 114, no. 5 (1991): 1069–78. http://dx.doi.org/10.1083/jcb.114.5.1069.

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The mouse progenitor T lymphocyte (pro-T) cell line FTF1 binds in vitro to thymus blood vessels, the thymic capsule, and liver from newborn mice. A mAb, EA-1, raised against an embryonic mouse endothelial cell line, blocked adhesion. The antibody also interfered with pro-T cell adhesion to a thymus-derived mouse endothelial cell line; it had no effect on the adhesion of mature T lymphocytes and myeloid cells. The antigen recognized by EA-1 is located on the vascular endothelium of various mouse tissues and absent on pro-T cells. EA-1 antibody precipitates molecules with apparent molecular weig

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Komatsu, Shunichiro, Rodney D. Berg, Janice M. Russell, Yuji Nimura, and D. Neil Granger. "Enteric microflora contribute to constitutive ICAM-1 expression on vascular endothelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 1 (2000): G186—G191. http://dx.doi.org/10.1152/ajpgi.2000.279.1.g186.

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Quantitative estimates of endothelial cell adhesion molecule expression have revealed that some adhesion molecules [e.g., intercellular adhesion molecule-1 (ICAM-1)] are abundantly expressed in different vascular beds under normal conditions. The objective of this study was to determine whether the enteric microflora contribute to the constitutive expression of ICAM-1 and other endothelial cell adhesion molecules in the gastrointestinal tract and other regional vascular beds. The dual radiolabeled monoclonal antibody technique was used to measure endothelial expression of ICAM-1, ICAM-2, vascu

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Wenisch, C. "Circulating selectins, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in hyperthyroidism." Journal of Clinical Endocrinology & Metabolism 80, no. 7 (1995): 2122–26. http://dx.doi.org/10.1210/jc.80.7.2122.

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Wenisch, C., D. Myskiw, A. Gessl, and W. Graninger. "Circulating selectins, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in hyperthyroidism." Journal of Clinical Endocrinology & Metabolism 80, no. 7 (1995): 2122–26. http://dx.doi.org/10.1210/jcem.80.7.7541802.

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