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Anat Rec (Hoboken). 2019 Sep;302(9):1587-1593. doi: 10.1002/ar.24040. Epub 2019 Jan 13.

AIP1 Suppresses Transplant Arteriosclerosis Through Inhibition of Vascular Smooth Muscle Cell Inflammatory Response to IFNγ.

Qin L1,2, Min W3, Xin S1,2.

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Department of Vascular Surgery, The First Hospital of China Medical University, 155 Nanjing Bei Street, Shenyang, China.
Key Laboratory of Pathogenesis, Prevention and Therapeutics of Aortic Aneurysm, Liaoning Province, China.
Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, Connecticut.


IFNγ-induced vascular smooth muscle cells (VSMCs) inflammatory response plays a key role in transplant arteriosclerosis (TA). However, the mechanisms regulating this process remains poorly defined. Here, we show that ASK1-interacting protein 1 (AIP1) deletion markedly augments the expression of IFNγ-induced chemokines in mouse aortic allografts. Subsequently, donor arterial grafts from AIP1 deficient mice exhibited an accelerated development of TA. Furthermore, AIP1 knockdown significantly increased IFNγ signaling activation in cultured VSMCs and thus enhances chemokines production in response to IFNγ. Together, we conclude that AIP1 functions as an inhibitor of VSMCs inflammation by regulating IFNγ signaling and therefore suppresses TA progression. Our findings suggest that AIP1 might be a potential therapeutic target for chronic transplant rejection. Anat Rec, 302:1587-1593, 2019.


ASK1-interacting protein 1; inflammatory response; interferon gamma; transplantation arteriosclerosis; vascular smooth muscle cells


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