Related Experiment Video
Updated: Jan 2, 2026
Murine Cervical Aortic Transplantation Model using a Modified Non-Suture Cuff Technique
Published on: November 2, 2019
Influence of caveolin-1 and endothelial nitric oxide synthase on adventitial inflammation in aortic transplants
Johannes Mierke1, Marian Christoph2, Antje Augstein2
1Department of Internal Medicine and Cardiology, Herzzentrum Dresden, University Clinic, Technische Universität Dresden, Dresden, Germany. johannes.mierke@mailbox.tu‑dresden.de
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 caveolin‑1 (Cav‑1) and endothelial nitric oxide synthase (eNOS) were directly involved in neointimal proliferation.
Aims:
In the current study, we investigated the impact of Cav‑1 and eNOS on adventitial processes in a murine model.
Methods:
Denuded aortas from C57Bl6n (wild‑type [WT]), Cav‑1-/, eNOS-/, and Cav‑1-//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 Cav‑1-/ 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 (VEGF‑A) despite the lowest macrophage content. In contrast, the knockout aortas showed a decreased content of VEGF‑A as well as decreased expression of α-smooth muscle actin (α-‑SMA) in the tunica media, suggesting induced VSMC migration. Moreover, the WT aortas exhibited increased neovessel formation.
Conclusions:
Cav‑1 and eNOS inhibit adventitial macrophage‑derived inflammation and modulate its cellular function. The knockout of Cav‑1 and eNOS leads to a decreased expression of VEGF-A, with decreased neovessel formation and increased migration of VSMCs, which promote a proatherogenic phenotype.
