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dc.contributor.advisorLarson, Douglas F.en_US
dc.contributor.authorGansert, Diane Elizabeth*
dc.creatorGansert, Diane Elizabethen_US
dc.date.accessioned2012-06-11T20:51:38Z
dc.date.available2012-06-11T20:51:38Z
dc.date.issued2012
dc.identifier.urihttp://hdl.handle.net/10150/228442
dc.description.abstractHypertension is a disease characterized by increased activity of the Renin Angiotensin System (RAAS) and immune related vascular dysfunction. Angiotensin II (Ang II) is the final effector molecule of the RAAS and has numerous biologic activities that perpetuates vascular remodeling and inflammation. Ang II signaling of inflammatory cells may be due the presence of RAAS components on T lymphocytes. Many studies have shown the importance of pro-inflammatory T cell phenotypes, through cytokine analysis, in hypertensive models. However, the specific characterization of the RAAS on these phenotypes has yet to be determined. We sought to establish the expression of RAAS components on naïve T cell subsets and compare that to changes in expression that may be seen with AngII treatment and anti-CD3/28 stimulation. Here we find that AngII and anti-CD3/28 treatments significantly increase the expression of RAAS components on T cell populations.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectMedical Pharmacologyen_US
dc.titleIn Vitro Analysis of the Extracellular Expression of the Renin Angiotensin System on T Lymphocyte Populationsen_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelmastersen_US
dc.contributor.committeememberLarmonier, Nicolasen_US
dc.contributor.committeememberVanderah, Todden_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineMedical Pharmacologyen_US
thesis.degree.nameM.S.en_US
refterms.dateFOA2018-08-18T07:24:52Z
html.description.abstractHypertension is a disease characterized by increased activity of the Renin Angiotensin System (RAAS) and immune related vascular dysfunction. Angiotensin II (Ang II) is the final effector molecule of the RAAS and has numerous biologic activities that perpetuates vascular remodeling and inflammation. Ang II signaling of inflammatory cells may be due the presence of RAAS components on T lymphocytes. Many studies have shown the importance of pro-inflammatory T cell phenotypes, through cytokine analysis, in hypertensive models. However, the specific characterization of the RAAS on these phenotypes has yet to be determined. We sought to establish the expression of RAAS components on naïve T cell subsets and compare that to changes in expression that may be seen with AngII treatment and anti-CD3/28 stimulation. Here we find that AngII and anti-CD3/28 treatments significantly increase the expression of RAAS components on T cell populations.


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