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Thesis Advisor | Leblanc, Normand | |
Author | Omandac, Venea | |
Date Accessioned | 2017-01-24T23:09:15Z | |
Date Available | 2017-01-24T23:09:15Z | |
Date of Issue | 2015 | |
Identifier (URI) | http://hdl.handle.net/11714/605 | |
Description | Ca2+-activated Cl- channels (CaCCs) play an important role in vascular smooth muscle contraction. This channel has recently been linked to Pulmonary Arterial Hypertension (PAH) due to its significant contribution to vascular tone and remodeling. Evidence shows that CaCCs are integral to vascular muscle contraction and could potentially be involved in the enhanced vasoconstriction found in PAH patients. TMEM16A is a gene shown to encode for CaCC in native pulmonary artery smooth muscle cells (PASMCs). Regulation mediated by CaMKII and PIP2 was found to significantly decrease CaCC conductance. This review of literature discusses the significance of the regulation of CaCCs in developing new treatments to target PASMCs in hypertensive patients. Past research along with future directions of this study could significantly contribute to developing novel methods of treatment for Pulmonary Arterial Hypertension, othercardiovascular diseases, and even abnormal cell-proliferating diseases such as cancer. | |
Item Format | ||
Item Language | en_US | |
Language | en_US | |
Rights | In Copyright(All Rights Reserved) | |
Title | Role of the Regulation of Calcium-Activated Chloride Channels on Pulmonary Artery Smooth Muscle Cells in Treating Pulmonary Arterial Hypertension | |
Type | Thesis | |
Rights Holder | Author(s) | |
Department | Psychology | |
Department | Biology | |
Degree Level | Honors Thesis | |
Degree Name | Neuroscience | |
Degree Grantor | University of Nevada, Reno | |
Degree Grantor | University of Nevada, Reno |