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Relevant bibliographies by topics / Vascular cell adhesion molecule

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Academic literature on the topic 'Vascular cell adhesion molecule'

Author: Grafiati

Published: 28 May 2022

Last updated: 18 July 2025

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Journal articles on the topic "Vascular cell adhesion molecule"

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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 increases in expression of these adhesion molecules. In a fractionation study, approximately 7 kDa fraction showed peak activity. This activity was tolerant to heating and trypsin digestion. These results indicate thatH pyloriwater extract contains water-soluble, low-molecular, nonprotein substances which induce upregulation of adhesion molecules on human umbilical vein endothelial cells, suggesting that products ofH pylorimay elicit gastric mucosal inflammation by promoting expression of endothelial adhesion molecules.

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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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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 International Collaborating Clinics classification criteria for SLE and 40 age and sex-matched healthy controls were included. In patients, clinical examination was performed and SLE disease activity index was assessed. Serum endothelin-1 and soluble vascular cell adhesion molecule-1 levels were measured using ELISA kits. Results The mean ± standard deviation age of patients and controls was 31.91 ± 7.66 and 33.20 ± 10.08 years, respectively. Compared to healthy controls, serum soluble vascular cell adhesion molecule-1 (1023.8 ± 352.96 vs. 866.06 ± 109.91) and endothelin-1 (77.83 ± 16.27 vs. 54.45 ± 12.01) was significantly higher in SLE patients ( P = 0.003 and P < 0.001, respectively). The most common organs involved in patients were skin, joint and kidney. There were no significant differences in serum soluble vascular cell adhesion molecule-1 and endothelin-1 levels according to organ involvement, activity of disease and the conventional serum markers of disease activity ( P > 0.05). There was no significant correlation between disease activity, organ involvement and negative or positivity of autoantibodies as well as serum complement with endothelin-1 and vascular cell adhesion molecule-1 levels ( P > 0.05). Conclusions Although our study revealed higher serum soluble vascular cell adhesion molecule-1 and endothelin-1 levels in SLE patients compared to healthy controls, there were no significant correlations between their serum levels with organ involvement and disease activity.

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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 angiogenesis, and its molecular mechanisms of action in the endothelium. In the endothelium, PECAM-1 not only plays a role as an adhesion molecule but also participates in intracellular signalling pathways which have an impact on various cell adhesive mechanisms and endothelial nitric oxide synthase (eNOS) expression and activity. In addition, recent studies from our laboratory have revealed an important relationship between PECAM-1 and endoglin expression. Endoglin is an essential molecule during angiogenesis, vascular development and integrity, and its expression and activity are compromised in the absence of PECAM-1. In the present review we discuss the roles that PECAM-1 isoforms may play in modulation of endothelial cell adhesive mechanisms, eNOS and endoglin expression and activity, and angiogenesis.

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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 to COVID-19 disease severity and may contribute to coagulation dysfunction.

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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 model “nidus” after 6 weeks, and the tissue was harvested 1 to 84 days after radiosurgery. Control groups received sham irradiation. Immunofluorescence was used to study the expression of E-selectin and vascular cell adhesion molecule-1. RESULTS: Endothelial E-selectin expression was limited to regions receiving radiosurgery. E-selectin expression reached maximal expression at 24 hours after radiosurgery and was sustained for another 24 hours before gradually reducing to baseline at 84 days post-radiosurgery (P &lt; .01). Vascular cell adhesion molecule-1 expression remained at the baseline level for the first week; a 50% increase was observed at 21 days after radiosurgery, which was sustained for another 3 weeks before returning to the baseline at 84 days after radiosurgery (P &lt; .05). CONCLUSION: Radiosurgery stimulates early expression of E-selectin and delayed up-regulation of vascular cell adhesion molecule-1 on the endothelial surface of the AVM model nidus. Cell adhesion molecule expression may play an important role in the process leading to vascular obliteration after irradiation. These molecular alterations may be harnessed to promote thrombosis in the irradiated vasculature using a vascular targeting agent.

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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 molecule 1 (VCAM-1), ICAM-2, P-selectin, E-selectin, and platelet-endothelial cell adhesion molecule 1 (PECAM-1) in different vascular beds of normal (C57Bl/6) and RM-1 tumor-bearing mice. When corrected for endothelial surface area, the constitutive expression of selectins in tumor vessels was higher than that observed in other vascular beds. Both constitutive and induced expression of endothelial CAMs in peripheral vascular beds did not differ between normal and tumor-bearing mice. Within the tumor, the magnitude of the upregulation of P-selectin, ICAM-1, and VCAM-1 after TNF-α was similar to that within other vascular beds. E-selectin expression in tumors was refractory to TNF-α, whereas PECAM-1 and ICAM-2 expression were significantly reduced. Our findings suggest that the presence of a solid tumor does not influence endothelial CAM expression in other vascular beds and that the higher density of selectins in nonstimulated tumor vessels may promote the recruitment of rolling leukocytes in this tissue.

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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. Our results also demonstrated that Lf was reduced the expression of cell adhesion molecules on H/R-induced vascular inflammation mouse model. Lf significantly reduced the gene expression of pro-inflammatory cytokine such as IL-6, IL-1β and TNF-α in hypoxia-induced HUVECs. These results demonstrate that Lf inhibits the expression of cell adhesion molecules including ICAM-1, VCAM-1 and pro-inflammatory cytokines. It also suggests that Lf may play an important role in the development of drug for anti-vascular inflammation by inhibiting the expression of cell adhesion molecules.

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Dissertations / Theses on the topic "Vascular cell adhesion molecule"

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Brown, Marena Dessette. "Sickle cell-endothelial interactions : modulation of cell adhesion molecule expression." Diss., Georgia Institute of Technology, 1995. http://hdl.handle.net/1853/11306.

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Cooke, Vesselina G. "Role of Junctional Adhesion Molecule-A in vascular biology." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 147 p, 2008. http://proquest.umi.com/pqdweb?did=1495945061&sid=5&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Alapati, Anuja. "Small Organic Molecule Inhibition of Tumor Necrosis Factor-a Induced Vascular Cell Adhesion Molecule-1 Expression by Endothelial Cells." Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1375177527.

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Wu, Tao. "Structure-function analysis of vascular tethering molecules using atomic force microscope." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/31844.

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Thesis (Ph.D)--Mechanical Engineering, Georgia Institute of Technology, 2009.<br>Committee Chair: Zhu, Cheng; Committee Member: Barry, Bridgette; Committee Member: Boyan, Barbara; Committee Member: McEver, Rodger; Committee Member: McIntire, Larry. Part of the SMARTech Electronic Thesis and Dissertation Collection.

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Ramrakha, Punit Satyavrat. "Strategies to modulate leukocyte adherence to endothelium : inhibition of vascular cell adhesion molecule expression." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402448.

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Koßmann, Eugen Franz Josef [Verfasser]. "Vascular Cell Adhesion Molecule-1 (VCAM-1) modulates plasticity of human melanoma cells / Eugen Franz Josef Koßmann." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2021. http://d-nb.info/1233008927/34.

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Fukiage, Kenichi. "Expression of vascular cell adhesion molecule-1 indicates the differentiation potential of human bone marrow stromal cells." Kyoto University, 2010. http://hdl.handle.net/2433/120604.

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Mulgrew, Scott. "Fatty acid regulation of adhesion molecule expression in human vascular cells." Thesis, Robert Gordon University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526063.

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Gandhi, Neha Sureshchandra. "Molecular modelling of platelet endothelial cell adhesion molecule 1 and its interaction with glycosaminoglycans." Thesis, Curtin University, 2007. http://hdl.handle.net/20.500.11937/1513.

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The Platelet Endothelial Cell Adhesion Molecule 1 (PECAM-1) has many functions including its roles in leukocyte extravasation as part of the inflammatory response, and in the maintenance of vascular integrity through its contribution to endothelial cell-cell adhesion. Various heterophilic ligands of PECAM-1 have been proposed. The possible interaction of PECAM-1 with glycosaminoglycans (GAGs) is the focus of this thesis. The three dimensional structure of the extracellular immunoglobulin (Ig)-domains of PECAM-1 was constructed using homology modelling and threading methods. Potential heparin/heparan sulfate binding sites were predicted on the basis of their amino acid consensus sequences and a comparison with known structures of sulfate binding proteins. Heparin and other GAG fragments have been docked to investigate the structural determinants of their protein binding specificity and selectivity. It is predicted that two regions in PECAM-1 appear to bind heparin oligosaccharides. A high affinity binding region was located in Ig-domains 2 and 3 and a low affinity region was located in Ig-domains 5 and 6.These GAG binding regions are distinct from regions involved in PECAM-1 homophilic interactions. Docking of heparin fragments of different size revealed that fragments as small as a pentasaccharide appear to be able to bind to domains 2 and 3 with high affinity. Binding of longer heparin fragments suggests that key interactions can occur between six sulfates in a hexasaccharide with no further increase in binding affinity for longer fragments. Molecular dynamics simulations were also used to characterise and quantify the interactions of heparin fragments with PECAM-1. These simulations confirmed the existence of regions of high and low affinity for GAG binding and revealed that both electrostatic and van der Waals interactions determine the specificity and binding affinity of GAG fragments to PECAM-1. The simulations also suggested the existence of ‘open’ and ‘closed’ conformations of PECAM-1 around domains 2 and 3.

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Amos, Amanda Owings. "Regulation of cytokine-induced adhesion molecule expression and sickle erythrocyte adhesion to microvascular endothelial cells by intracellular adenosine 3',5'-cyclic monophosphate and nitric oxide." Diss., Available online, Georgia Institute of Technology, 2006, 2006. http://etd.gatech.edu/theses/available/etd-04052006-104355/.

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Thesis (Ph. D.)--Chemical and Biomolecular Engineering, Georgia Institute of Technology, 2006.<br>Dr. Peter A. Lane, Committee Member ; Dr. Larry V. McIntire, Committee Member ; Dr. Ronald W. Rousseau, Committee Member ; Dr. James R. Eckman, Committee Member ; Dr. Timothy M. Wick, Committee Chair.

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Books on the topic "Vascular cell adhesion molecule"

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D, Pearson Jeremy, ed. Vascular adhesion molecules and inflammation. Birkhäuser, 1999.

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D, Pearson Jeremy, ed. Vascular adhesion molecules and inflammation. Birkhäuser, 1999.

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L, Gordon J., ed. Vascular endothelium: Interactions with circulating cells. Elsevier, 1991.

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Bereta, Joanna. Regulation of expression of vascular cell adhesion molecule-1 and inducible nitric oxide synthase in murine brain microvascular endothelium. Wydawn. Uniwersytetu Jagiellońskiego, 1997.

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Dominique, Bagnard, ed. Neuropilin: From nervous system to vascular and tumor biology. Kluwer Academic/Plenum Pub., 2002.

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Dominique, Bagnard, ed. Neuropilin: From nervous system to vascular and tumor biology. Kluwer Academic/Plenum Pub., 2002.

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Dominique, Bagnard, ed. Neuropilin: From nervous system to vascular and tumor biology. Kluwer Academic/Plenum Pub., 2002.

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Gallagher, Helen Christine. Regulation of neural cell adhesion molecule polysialylation state. University College Dublin, 1998.

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Berezin, V. A. Structure and function of the neural cell adhesion molecule NCAM. Springer, 2010.

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Berezin, Vladimir, ed. Structure and Function of the Neural Cell Adhesion Molecule NCAM. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1170-4.

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Book chapters on the topic "Vascular cell adhesion molecule"

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Salajegheh, Ali. "Vascular Cell Adhesion Molecule-1 (VCAM-1)." In Angiogenesis in Health, Disease and Malignancy. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_59.

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Qidwai, Tabish. "Vascular Cell Adhesion Molecule-1 (VCAM-1) Polymorphisms." In Exploration of Host Genetic Factors associated with Malaria. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4761-8_14.

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Clements, J. M., R. Pigott, L. A. Needham, and A. J. H. Gearing. "Adhesion molecules in disease: vascular cell adhesion molecule-1 as a target for therapy." In The Vasculitides. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-2889-4_6.

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Derosa, Giuseppe, and Pamela Maffioli. "Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression in Liver Disease." In Biomarkers in Disease: Methods, Discoveries and Applications. Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7675-3_24.

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Derosa, Giuseppe, and Pamela Maffioli. "Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression in Liver Disease." In Biomarkers in Disease: Methods, Discoveries and Applications. Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7742-2_24-1.

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Yoshikawa, Toshikazu, Norimasa Yoshida, Hiroki Manabe, Yoshimitsu Terasawa, Toshiki Takemura, and Motoharu Kondo. "Effect of α-Tocopherol on Expression of Intercellular Adhesion Molecule-1 and Vascular Adhesion Molecule-1 on Human Vascular Endothelial Cells." In Food Factors for Cancer Prevention. Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-67017-9_91.

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Blease, Kate, Paul G. Hellewell, and Anne C. Burke-Gaffney. "Expression and Functional Consequences of Cytokine- or Lipopolysaccharide-Induced Adhesion Molecule Expression on Human Lung Microvascular Endothelial Cells." In Vascular Endothelium. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_19.

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Khandoga, A., S. Hüttinger, A. G. Khandoga, et al. "The role of Endothelial Cell-Selective Adhesion Molecule (ESAM) for leukocyte migration and vascular permeability during hepatic ischemia-reperfusion." In Deutsche Gesellschaft für Chirurgie. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_61.

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Sato, Thomas N., and Ying Qin. "A Novel Gene Family May Encode Endothelial Cell Specific Adhesion-Like Molecules: An Extracellular Loop-Repeat-Loop (LRL) Motif and Cytoplasmic Tyrosine Kinase Domains." In Frontiers in Cerebral Vascular Biology. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2920-0_29.

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Holdenrieder, S., and P. Stieber. "Neural Cell Adhesion Molecule." In Lexikon der Medizinischen Laboratoriumsdiagnostik. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_2245-1.

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Conference papers on the topic "Vascular cell adhesion molecule"

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Weidert, Eric, Payal Khanna, Francisco Vital-Lopez, and Cheng Dong. "Model Simulations Reveal VCAM-1 Augment PAK Activation Rates to Amplify p38 MAPK and VE-Cadherin Phosphorylation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80364.

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Metastasis is a complex process mediated by both adhesion molecules and chemokine secretion [1]. One important event during cancer metastasis is tumor cell extravasation through the endothelium [1]. In melanoma cancer, tumor cell extravasation is mediated by very late antigen (VLA)-4 molecule adhesion to vascular cell adhesion molecules (VCAM)-1 on endothelial cells [2]. High expression levels of VLA-4 integrin are associated with a marked increase in melanoma extravasation through endothelial layers [2]. The binding of VLA-4 to VCAM -1 induces the activation of downstream mitogen activated protein kinase (MAPK) signaling cascades, which regulate the vascular endothelial (VE)-cadherin junctions that hold together endothelial cells [2].

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Rossi, Joanna, Léonie Rouleau, Jean-Claude Tardif, and Richard L. Leask. "Fluid Shear Stress Reduces Simvastatin Induced Adhesion Molecule Expression in Cytokine Activated Endothelial Cells." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206539.

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Although originally designed as inhibitors of cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, are now known to also have non-lipid lowering benefits [1]. Statins have been reported to modulate gene expression in endothelial cells, however, the effect of statins on adhesion molecule expression is contradictory. Some studies report a decrease in adhesion molecule mRNA and/or protein after statin treatment [2], while others have shown that statins potentiate the effect of tumor necrosis factor alpha (TNFα) [3]. To the best of our knowledge, the effects of statins on gene expression in cultured endothelial cells has been done in static conditions only and no study has examined the effect of blood flow. This is particularly important since fluid shear stress is a strong regulator of endothelial cell function and phenotype [4]. The purpose of this study was to clarify the effects of statins on vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) expression in endothelial cells by evaluating their biological response under fluid flow.

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Imai, Yohsuke, Hitoshi Kondo, Young Ho Kang, Takuji Ishikawa, Chwee Teck Lim, and Takami Yamaguchi. "A Numerical Model of Adhesion Property of Malaria Infected Red Blood Cells in Micro Scale Blood Flows." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206456.

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Infection by malaria parasite changes mechanical properties of red blood cells (RBCs). Infected red blood cells (IRBCs) lose the deformability but also develop the ability to cytoadhere and rosetting. These outcomes can lead to microvascular blockage [1]. The stiffness of IRBCs [2] and its effects on the flow in micro channels [3] were studied with recent experimental techniques. The cytoadherence and rosetting properties of IRBCs have also been studied experimentally. The cytoadherence is mediated by the interaction of the parasite protein PfEMP1 with several endothelial adhesion molecules, such as CD36, intercellular adhesion molecule-1 (ICAM-1), P-selectin, and vascular cell adhesion molecule-1 (VCAM-1) [4]. In particular, the ligand-receptor interaction between PfEMP1 and CD36 shows tight adhesion [5]. Microvascular blockage may be a hemodynamic problem, involving the interactions between IRBCs, healthy RBCs (HRBCs) and endothelial cells (ECs) in flowing blood, but however experimental techniques have several limitations to this topic. First, it is still difficult to observe the RBC behavior interacting with many other cells even with the recent confocal microscopy. Second, the three-dimensional information on flow field is hardly obtained. Third, capillaries in human body are circular channels with complex geometry, but such complex channels cannot be created in micro scale. Instead, numerical modeling can overcome these problems. We presented a two-dimensional hemodynamic model involving adhesive interactions [6]. In this paper, we propose a three-dimensional model of the adhesive interactions for micro scale hemodynamics in malaria infection.

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Al-Mrabt, N., TA Martin, and WG Jiang. "Abstract P1-02-03: JAM-2, Junctional Adhesion Molecule-2 Influences the Adhesion and Migration of Vascular Endothelial Cell." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p1-02-03.

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Kopacz, Adrian M., Brandon J. Tefft, Shu Q. Liu, and Wing K. Liu. "Modeling of Endothelial Cell Adhesion Dynamics Modulated by Molecular Engineering." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13269.

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Vascular thrombosis, intimal hyperplasia, and atherosclerosis are common disorders affecting a very large portion of the human population. A potential reduction in these disorders will elicit a significant impact. It has been shown that endothelial cells play a critical role in protecting blood vessels against the formation of thrombosis and atherosclerosis. Hence, a successful endothelial cell lining of arterial constructs will prevent intimal hyperplasia in reconstructed arteries. However, in practice endothelial cells often detach from reconstructed arteries due to weak adhesion strength, hindering the effectiveness of endothelial cell lining.

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Gimbrone, M. A., M. P. Bevilacqua, and M. E. Wheeler. "ENDOTHELIAL-DEPENDENT MECHANISMS OF LEUKOCYTE ADHESION: ROLE OF MONOKINES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643983.

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Localized adhesion of peripheral blood leukocytes to the vessel wall is an essential component of inflammatory reactions. There is increasing experimental evidence that vascular endothelial cells play an active role in this process. Our laboratory has been especially interested in defining endothelial-dependent mechanisms of leukocyte adhesion, and the role of leukocyte products in their modulation. We have reported1 that purified natural human monocyte-derived interleukin 1 (IL-1) can act directly on cultured human endothelial cells (HEC) to dramatically increase the adhesiveness of their surfaces for human polymorphonuclear leukocytes (PMN), monocytes and the related cell lines HL-60 and U937. This effect was concentration-, time- (onset≅30 min; peak≅4h) , and protein/RNA-synthesis-requiring, and, in selective pretreatment/fixation experiments, was shown to be mediated primarily through the endothelial cell. To better define this inducible endothelial pro-adhesive mechanism, we have developed a series of murine monoclonal antibodies directed against monokine-stimulated HEC surfaces. One of these antibodies (H4/18) recognizes an endothelial cell surface structure which is induced by IL-1 (and certain other cytokines)2 in a similar fashion (kinetics, concentration - dependence, sensitivity to metabolic inhibitors) as the pro-adhesive surface change for leukocytes. H4/18 partially blocks HD-60 cell adhesion to monokine-treated HEC, and, in vivo, labels human vascular endothelium at sites of experimental delayed hypersensitivity reactions4. A second monoclonal antibody (H18/7)5 significantly blocks the adhesion of both HL-60 cells and PMN to monokine-treated HEC. Monoclonal antibodies H4/18 and H18/7 appear to recognize the same inducible surface structure as assessed by immunoprecipitation of extracts of metabolically labeled, monokine-stimulated HEC. We have designated this monokine-inducible, endothelial-leukocyte adhesion molecule "E-IAM 1". IL-1 treated HEC cultures (in contrast to sham-treated control cultures) generate a soluble leukocyte adhesion inhibitor (LAI)6,7. LAI acts on PMN to inhibit their adhesion to hyperadhesive endothelial monolayers as well as to serum-coated plastic surfaces, but does not inhibit PMN activation by chemotactic stimuli (LTB4, f-met-leu-phe). IAI appears to differentially inhibit adhesion of peripheral blood leukocytes, isolated from the same donor, to hyperadhesive HEC (PMN > monocytes; lymphocytes, no effect), and does not inhibit HL-60 cell-HEC adhesion. Endothelial production of IAI is time-dependent (peak 5-6 h.), and blocked by cycloheximide but not by aspirin. Preliminary characterization indicates that LAI is nonsedimentable (250,000 xg, 45 min), nondialyzable (>10 kD), stable to heat (80°C, 30 min) and acid (pH 2) and is precipitable by ammonium sulphate (60-80% saturation). Thus, this endothelial-derived inhibitory activity, which appears to be distinct from PGI2 or other cyclooxygenase products, blocks leukocyte adhesion without globally suppressing leukocyte function. Further characterization of the cellular and molecular mechanisms regulating the endothelial expression of E-LAM 1 and LAI should contribute to our understanding of the active role of the vascular wall in the inflammatory process.1. Bevilacqua et al. (1985); J. Clin. Invest.76:2003.2. Cotran et al. (1986); J. Exp. Med. 164:661.3. Bevilacqua et al. (1987); Fed. Proc. (in press).4. Wheeler et al. (1986); Fed. Proc. 45:1725.5. Wheeler et al. (1987); Fed. Proc. (in press).

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Graham, Drew A., Danil V. Dobrynin, Alexander Fridman, Gary Friedman, and Alisa Morss Clyne. "A Pin-to-Hole Spark Discharge Plasma Generates Nitric Oxide and Can Be Safely Applied to an Endothelial Cell Monolayer." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206764.

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Endothelial cells line all blood vessels and regulate many homeostatic functions (e.g. platelet aggregation, vascular tone, vascular cell proliferation, leukocyte adhesion) by production of the signaling molecule nitric oxide (NO). NO bioavailability and thus endothelial cell function are compromised in many chronic disease states, including diabetes mellitus and its associated micro- and macrovascular complications (e.g. impaired wound healing and atherosclerosis, respectively) [1]. In the specific case of diabetic wound healing, application of exogenous NO to the diseased tissue may help restore critical NO-mediated processes and could positively impact healing and overall patient health [2]. We have developed a novel pin-to-hole spark discharge plasma device that generates NO and can be applied to cultured endothelial cells with minimal cell injury or death. We propose that this plasma device represents a promising novel method for topical NO application.

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Henretta, Melissa, Jennifer M. Scalici, Linda Duska, Jill Slack-Davis, and Kristen Atkins. "Abstract 845: Vascular cell adhesion molecule-1 (VCAM-1) expression in patients with ovarian tumors of low malignant potential." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-845.

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Oleszowsky, Mara, Widian Laaraj, Tanja Kottmann, and Matthias Seidel. "AB1330 SOLUBLE VASCULAR CELL ADHESION MOLECULE-1 AS AN INDEPENDENT MARKER FOR ENDOTHELIAL ACTIVATION IS ELEVATED IN ACTIVE RHEUMATIC DISEASES: A MULTIVARIATE ANALYSIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3085.

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Sanders, Andrew James, David Guo Jiang, Jianyuan Zeng, et al. "Abstract PS17-48: Potential role of activated leukocyte cell adhesion molecule (ALCAM) in hepatocyte growth factor (HGF) signalling in vascular endothelial cells and implications in breast cancer." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps17-48.

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Reports on the topic "Vascular cell adhesion molecule"

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Lin, Sue-Hwa. Tumor Specific Regulation of C-CAM Cell Adhesion Molecule in Prostate Cancer Carcinogenesis. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada393974.

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Resnick, Nicole M. The Expression and Regulation of the Cell Adhesion Molecule CD44 in Human Breast Cancer. Defense Technical Information Center, 1995. http://dx.doi.org/10.21236/ada300406.

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Mahanonda, Rangsini, Orawan Charatkulangkun, and Sathit Pichyangkul. The role of IL-17 in periodontitis. Chulalongkorn University, 2006. https://doi.org/10.58837/chula.res.2006.12.

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Background and objectives: IL-17 is a novel T cell-derived cytokine that promotes inflammatory responses. It is presence in inflamed gingival tissues and gingival crevicular fluid of periodontitis patients. In this study we investigated the effects of IL-17 alone or in combination with IFN-Y on the immune modulation of human gingival fibroblasts (HGFs) which would contribute to pathogenesis of periodontium. Methods and results: Various concentrations of IL-17, IFN-Y or the combination of these two cytokines were added to HGF cultures. The expression of ICAM-1, HLA-DR, and CD40 was assessed by flow cytometry and IL-8 production was determined by ELISA. Our results demonstrated that IFN-Y markedly induced expression of HLA-DR and ICAM-1 and slightly induced CD40 expression on HGFs. In contrast, IL-17 had no effect on these molecules. When combined, IL-17 did not enhance IFN-Y-induced HLA-DR and CD40 expression but significantly up-regulated ICAM-1 expression (p<0.01), Unlike IFN-Y, IL-17 induced IL-8 production from HGFs. When combined, IFN-Y synergistically enhanced IL-17-induce IL-8 production in all HGF lines (p<0.05). Conclusions: These findings indicate that IL-17 and IFN-Y have different effects on HGFs regarding the expression of co-stimulatory molecule and adhesion molecule as well as immune mediator. All of these molecules are critical in controlling immune response, thus indicating the immunoregulatory role of locally produced IL-17 and IFN-Y in inflamed periodontal tissue.

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