| First Author | Fang J | Year | 2019 |
| Journal | Inflammation | Volume | 42 |
| Issue | 4 | Pages | 1190-1202 |
| PubMed ID | 30806956 | Mgi Jnum | J:294494 |
| Mgi Id | MGI:6456450 | Doi | 10.1007/s10753-019-00979-2 |
| Citation | Fang J, et al. (2019) alpha7nAChR Deletion Aggravates Myocardial Infarction and Enhances Systemic Inflammatory Reaction via mTOR-Signaling-Related Autophagy. Inflammation 42(4):1190-1202 |
| abstractText | Alpha7 nicotinic acetylcholine receptor (alpha7nAChR) has been previously reported to play an alleviative role in myocardial infarction (MI). In this study, we investigated its specific mechanism. alpha7nAChR(-/-) mice and its control (alpha7nAChR(+/+)) were used for the study of alpha7nAChR. Left anterior descending coronary artery occlusion was conducted for the creation of mice MI model and lipopolysaccharide (LPS) was used as inflammatory stressor in murine peritoneal macrophages. Triphenyltetrazolium chloride (TTC) staining and echocardiography was used for the detection of infarct size and cardiac function, respectively. Western blot was conducted for the testing of autophagy-related proteins and enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR) was used for the testing of proinflammatory cytokines. Rapamycin was used for the induction of autophagy through inhibiting mammalian target of rapamycin (mTOR)-related signaling. We found that knocking out alpha7nAChR enhanced the cardiac infarct size and damaged cardiac function in MI. alpha7nAChR deficiency increased the levels of several proinflammatory cytokines in serum and spleen from MI mice as well as murine macrophages under inflammatory stress. alpha7nAChR deletion decreased the level of autophagy in spleen from MI mice and macrophages under inflammatory stress. Rapamycin alleviated the cardiac function and systemic inflammatory reaction in MI mice as well as inflammatory reaction in macrophages under inflammatory stress, which was attenuated by knocking out alpha7nAChR. Our current study investigated the mechanism of alpha7nAChR-mediated cardio-protective and anti-inflammatory effect related to mTOR-related autophagy, which might provide a novel insight in the treatment of MI. |
