Interferon regulatory factor 9 is critical for neointima formation following vascular injury

Shu-Min Zhang, Li-Hua Zhu, Hou-Zao Chen, Ran Zhang, Peng Zhang, Ding-Sheng Jiang, Lu Gao, Song Tian, Lang Wang, Yan Zhang, Pi-Xiao Wang, Xiao-Fei Zhang, Xiao-Dong Zhang, Liu De-Pei () and Hongliang Li ()
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Shu-Min Zhang: Renmin Hospital of Wuhan University
Li-Hua Zhu: Renmin Hospital of Wuhan University
Hou-Zao Chen: State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College
Ran Zhang: State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College
Peng Zhang: Renmin Hospital of Wuhan University
Ding-Sheng Jiang: Renmin Hospital of Wuhan University
Lu Gao: Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
Song Tian: Cardiovascular Research Institute, Wuhan University
Lang Wang: Renmin Hospital of Wuhan University
Yan Zhang: Renmin Hospital of Wuhan University
Pi-Xiao Wang: Renmin Hospital of Wuhan University
Xiao-Fei Zhang: College of Life Sciences, Wuhan University
Xiao-Dong Zhang: College of Life Sciences, Wuhan University
Liu De-Pei: State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College
Hongliang Li: Renmin Hospital of Wuhan University

Nature Communications, 2014, vol. 5, issue 1, 1-17

Abstract: Abstract Interferon regulatory factor 9 (IRF9) has various biological functions and regulates cell survival; however, its role in vascular biology has not been explored. Here we demonstrate a critical role for IRF9 in mediating neointima formation following vascular injury. Notably, in mice, IRF9 ablation inhibits the proliferation and migration of vascular smooth muscle cells (VSMCs) and attenuates intimal thickening in response to injury, whereas IRF9 gain-of-function promotes VSMC proliferation and migration, which aggravates arterial narrowing. Mechanistically, we show that the transcription of the neointima formation modulator SIRT1 is directly inhibited by IRF9. Importantly, genetic manipulation of SIRT1 in smooth muscle cells or pharmacological modulation of SIRT1 activity largely reverses the neointima-forming effect of IRF9. Together, our findings suggest that IRF9 is a vascular injury-response molecule that promotes VSMC proliferation and implicate a hitherto unrecognized ‘IRF9–SIRT1 axis’ in vasculoproliferative pathology modulation.

Date: 2014
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DOI: 10.1038/ncomms6160

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