| First Author | Luan P | Year | 2019 |
| Journal | Nat Commun | Volume | 10 |
| Issue | 1 | Pages | 2882 |
| PubMed ID | 31253783 | Mgi Jnum | J:283449 |
| Mgi Id | MGI:6323851 | Doi | 10.1038/s41467-019-10784-y |
| Citation | Luan P, et al. (2019) NLRC5 inhibits neointima formation following vascular injury and directly interacts with PPARgamma. Nat Commun 10(1):2882 |
| abstractText | NLR Family CARD Domain Containing 5 (NLRC5), an important immune regulator in innate immunity, is involved in regulating inflammation and antigen presentation. However, the role of NLRC5 in vascular remodeling remains unknown. Here we report the role of NLRC5 on vascular remodeling and provide a better understanding of its underlying mechanism. Nlrc5 knockout (Nlrc5(-/-)) mice exhibit more severe intimal hyperplasia compared with wild-type mice after carotid ligation. Ex vivo data shows that NLRC5 deficiency leads to increased proliferation and migration of human aortic smooth muscle cells (HASMCs). NLRC5 binds to PPARgamma and inhibits HASMC dedifferentiation. NACHT domain of NLRC5 is essential for the interaction with PPARgamma and stimulation of PPARgamma activity. Pioglitazone significantly rescues excessive intimal hyperplasia in Nlrc5(-/-) mice and attenuates the increased proliferation and dedifferentiation in NLRC5-deficient HASMCs. Our study demonstrates that NLRC5 regulates vascular remodeling by directly inhibiting SMC dysfunction via its interaction with PPARgamma. |
