| First Author | Johansson ME | Year | 2014 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 34 |
| Issue | 12 | Pages | 2632-6 |
| PubMed ID | 25324572 | Mgi Jnum | J:230459 |
| Mgi Id | MGI:5760105 | Doi | 10.1161/ATVBAHA.114.303892 |
| Citation | Johansson ME, et al. (2014) alpha7 Nicotinic acetylcholine receptor is expressed in human atherosclerosis and inhibits disease in mice--brief report. Arterioscler Thromb Vasc Biol 34(12):2632-6 |
| abstractText | OBJECTIVE: Cholinergic pathways of the autonomic nervous system are known to modulate inflammation. Because atherosclerosis is a chronic inflammatory condition, we tested whether cholinergic signaling operates in this disease. We have analyzed the expression of the alpha7 nicotinic acetylcholine receptor (alpha7nAChR) in human atherosclerotic plaques and studied its effects on the development of atherosclerosis in the hypercholesterolemic Ldlr(-/-) mouse model. APPROACH AND RESULTS: alpha7nAChR protein was detected on T cells and macrophages in surgical specimens of human atherosclerotic plaques. To study the role of alpha7nAChR signaling in atherosclerosis, male Ldlr(-/-) mice were lethally irradiated and reconstituted with bone marrow from wild-type or alpha7nAChR-deficient animals. Ablation of hematopoietic cell alpha7nAChR increased aortic atherosclerosis by 72%. This was accompanied by increased aortic interferon-gamma mRNA, implying increased Th1 activity in the absence of alpha7nAChR signaling. CONCLUSIONS: The present study shows that signaling through hematopoietic alpha7nAChR inhibits atherosclerosis and suggests that it operates by modulating immune inflammation. Given the observation that alpha7nAChR is expressed by T cells and macrophages in human plaques, our findings support the notion that cholinergic regulation may act to inhibit disease development also in man. |
