Hypertension 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.
| Identifer | oai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/228442 |
| Date | January 2012 |
| Creators | Gansert, Diane Elizabeth |
| Contributors | Larson, Douglas F., Larmonier, Nicolas, Vanderah, Todd |
| Publisher | The University of Arizona. |
| Source Sets | University of Arizona |
| Language | English |
| Detected Language | English |
| Type | text, Electronic Thesis |
| Rights | Copyright © 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. |
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