NLRC5 inhibits neointima formation following vascular injury and directly interacts with PPARγ

Peipei Luan, Weixia Jian, Xu Xu, Wenxin Kou, Qing Yu, Handan Hu, Dali Li, Wei Wang, Mark W. Feinberg, Jianhui Zhuang (), Yawei Xu () and Wenhui Peng ()
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Peipei Luan: Tongji University
Weixia Jian: School of Medicine
Xu Xu: Tongji University
Wenxin Kou: Tongji University
Qing Yu: Tongji University
Handan Hu: East China Normal University
Dali Li: East China Normal University
Wei Wang: Columbia University Medical Center
Mark W. Feinberg: Harvard Medical School
Jianhui Zhuang: Tongji University
Yawei Xu: Tongji University
Wenhui Peng: Tongji University

Nature Communications, 2019, vol. 10, issue 1, 1-16

Abstract: Abstract 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 PPARγ and inhibits HASMC dedifferentiation. NACHT domain of NLRC5 is essential for the interaction with PPARγ and stimulation of PPARγ 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 PPARγ.

Date: 2019
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DOI: 10.1038/s41467-019-10784-y

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