The renin-angiotensin system (RAS) has been implicated in vascular inflammation and atherosclerosis. Angiotensin II via the ATR1 can activate monocytes to produce inflammatory factors and increase adhesion. ATR1 expression is partly regulated by alternate splicing of the ATR1 gene. The RAS may also regulate immune function as part of the stress response: a model is proposed.
ATR1 expression in two monocyte cell lines (U937 and THP-1) compared to a human microvascular endothelial cell line (HMEC1) was investigated. Western blot showed ATR1 protein expression in all cell types. PCR protocols targeted to the terminal protein-coding exon common to all transcript variants confirmed mRNA expression of the ATR1 gene in EC and monocytes. The 5 known splice variants were not identified in monocytes. 5-RLM RACE was used to identify the 5 untranslated ATR1 exons in monocytes. These data suggest a novel monocyte-specific splice variant, which may function in the cardiovascular disease process.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:AEU.10048/650 |
| Date | 11 1900 |
| Creators | Groeschel, Michael |
| Contributors | Braam, Branko (Physiology, Nephrology), Karpinski, Edward (Physiology), Ballermann, Barbara (Physiology, Nephrology), Murray, Allan (Nephrology) |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | Thesis |
| Format | 4669350 bytes, application/pdf |
Page generated in 0.0023 seconds