| First Author | Mierke J | Year | 2020 |
| Journal | Kardiol Pol | Volume | 78 |
| Issue | 2 | Pages | 124-130 |
| PubMed ID | 31790082 | Mgi Jnum | J:328424 |
| Mgi Id | MGI:6719632 | Doi | 10.33963/KP.15079 |
| Citation | Mierke J, et al. (2020) Influence of caveolin-1 and endothelial nitric oxide synthase on adventitial inflammation in aortic transplants. Kardiol Pol 78(2):124-130 |
| abstractText | BACKGROUND: Restenosis after endovascular interventions is a clinically relevant process that is directly associated with increased morbidity. Thereby, an increased migration and proliferation of vascular smooth muscle cells (VSMCs) is mainly responsible for recurrent lumen narrowing. Previously, we showed that caveolin1 (Cav1) and endothelial nitric oxide synthase (eNOS) were directly involved in neointimal proliferation. AIMS: In the current study, we investigated the impact of Cav1 and eNOS on adventitial processes in a murine model. METHODS: Denuded aortas from C57Bl6n (wildtype [WT]), Cav1-/, eNOS-/, and Cav1-//eNOS-/ mice were transplanted into common carotid arteries of WT mice. The explantation was performed after 6 weeks, followed by Elastica van Gieson staining and immunohistochemistry. RESULTS: The Cav1-/ and the eNOS-/ aortas showed an increase in the adventitial content of macrophages, whereas their combined knockout did not lead to additive effects. Differences were observed despite the same acceptor, suggesting the local origin of inflammatory cells. Furthermore, the WT transplants exhibited the highest content of vascular endothelial growth factor A (VEGFA) despite the lowest macrophage content. In contrast, the knockout aortas showed a decreased content of VEGFA as well as decreased expression of alpha-smooth muscle actin (alpha-SMA) in the tunica media, suggesting induced VSMC migration. Moreover, the WT aortas exhibited increased neovessel formation. CONCLUSIONS: Cav1 and eNOS inhibit adventitial macrophagederived inflammation and modulate its cellular function. The knockout of Cav1 and eNOS leads to a decreased expression of VEGF-A, with decreased neovessel formation and increased migration of VSMCs, which promote a proatherogenic phenotype. |
