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dc.contributor.authorRooney, Meghanen
dc.date2013-10-10 15:34:51.802
dc.date.accessioned2013-10-15T22:20:34Z
dc.date.available2013-10-15T22:20:34Z
dc.date.issued2013-10-15
dc.identifier.urihttp://hdl.handle.net/1974/8420
dc.descriptionThesis (Master, Chemical Engineering) -- Queen's University, 2013-10-10 15:34:51.802en
dc.description.abstractSmall diameter synthetic vascular grafts have yet to be clinically successful due to luminal narrowing from thrombosis and intimal hyperplasia. Current attempts to address this issue include the development of materials that support endothelialisation and protein modification to the material surfaces that reduce thrombosis. The extracellular matrix protein elastin has been found to be one of the least thrombogenic components of blood vessels, and its purified and recombinant forms have shown reduced thrombogenicity in both in vitro and in vivo models. Biomaterial coatings of elastin-like polypeptides (ELPs) recombinantly produced in the Woodhouse laboratory showed reduced fibrinogen adsorption, platelet adhesion, and platelet activity. However, the reason for their relative non-thrombogenicity is still not fully understood. In this work, the leukocyte response to ELP-coated materials was investigated. In particular, ELP1 and ELP4, which differ in molecular weight and sequence length, were physically adsorbed to a polyethylene terephthalate surface (MylarTM), yielding 0.22 ± 0.13 μg/cm2 and 0.37 ± 0.19 μg/cm2 surface coverage, respectively, as determined by the colorimetric assay, FastinTM Elastin. These surfaces were exposed to flowing citrated whole blood for surface and bulk evaluation of leukocyte activity using scanning electron microscopy and flow cytometry, respectively. Little leukocyte activation was observed on the surface of the controls, low-density polyethylene and uncoated MylarTM. In the bulk, tissue factor (TF) expression (monocytes: ELP1 = 38.6 ± 16.3 %, ELP4 = 33.9 ± 18.1 %) and platelet-leukocyte aggregates determined by CD61 (monocytes: ELP1 = 63.1 ± 17.1 %, ELP4 = 61.8 ± 16.8 %; granulocytes: ELP1 = 62.7 ± 17.0 %, ELP4 = 60.5 ± 20.1 %) were both decreased compared to uncoated MylarTM, while CD11b upregulation (monocytes: ELP1 = 18.7 ± 2.2 %, ELP4 = 19.7 ± 2.7 %; granulocytes: ELP = 21.4 ± 3.7 %, ELP4 = 22.0 ± 3.2 %) was increased. The statistical dependence of TF expression and platelet-monocyte aggregates was tested; however, no correlation was found. Overall, platelet-leukocyte aggregate formation was reduced and there were conflicting results with regards to the reduction of leukocyte activation for the ELP coatings on MylarTM.en
dc.language.isoengen
dc.relation.ispartofseriesCanadian thesesen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectelastin-like polypeptidesen
dc.subjectcone and plateen
dc.subjectblood-contacting devicesen
dc.subjectshear rateen
dc.subjectleukocytesen
dc.subjecttissue factoren
dc.subjectCD11ben
dc.subjectelastinen
dc.titleLeukocyte Response to Elastin-Like Polypeptide Coatingsen
dc.typethesisen
dc.description.degreeM.A.Sc.en
dc.contributor.supervisorWoodhouse, Kimberlyen
dc.contributor.departmentChemical Engineeringen
dc.degree.grantorQueen's University at Kingstonen


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