| First Author | Sales VL | Year | 2005 |
| Journal | Circulation | Volume | 112 |
| Issue | 21 | Pages | 3328-36 |
| PubMed ID | 16286588 | Mgi Jnum | J:116912 |
| Mgi Id | MGI:3695213 | Doi | 10.1161/CIRCULATIONAHA.105.541714 |
| Citation | Sales VL, et al. (2005) Angiotensin type 2 receptor is expressed in murine atherosclerotic lesions and modulates lesion evolution. Circulation 112(21):3328-36 |
| abstractText | BACKGROUND: In the vasculature, the angiotensin type 2 (AT2) receptor (AT2R) exerts antiproliferative, antifibrotic, and proapoptotic effects. Normal adult animals have low AT2R expression; however, vascular injury and exposure to proinflammatory cytokines augment AT2R levels. We hypothesized that AT2R expression increases during initiation and progression of atherosclerosis. METHODS AND RESULTS: Atherosclerotic lesions of apolipoprotein (Apo) E(-/-) mice contained AT2Rs, measured by real-time polymerase chain reaction and confirmed by immunohistochemistry. To test the consequences of this expression, male ApoE(-/-), angiotensin II type 2 receptor-deficient (Agtr2-), and ApoE(-/-), wild-type (Agtr2+) mice consumed a high-cholesterol diet from 4 weeks of age. Ten weeks later, overall area and cellular composition of aortic arch lesions did not differ significantly among genotypes. After 16 weeks, ApoE(-/-)/Agtr2+, but not ApoE(-/-)/Agtr2- mice had dramatic decreases in percent positive area of macrophages, smooth muscles, lipids, and collagen. Diminished bromodeoxyuridine incorporation and increased TUNEL staining accompanied these decreases. CONCLUSIONS: Thus, loss of AT2R during the evolution of atherosclerotic lesions augmented the extent of cellularity of atherosclerotic lesions, establishing AT2R as a modulator of atherogenesis. |
