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5‐Aminoimidazole‐4‐carboxamide 1‐β‐D‐ribofuranoside reduces intimal hyperplasia of tissue engineering blood vessel by inhibiting phenotype switch of vascular smooth muscle cell
Author(s) -
Wu Yangxiao,
Liu Ge,
Chen Wen,
Yang Mingcan,
Zhu Chuhong
Publication year - 2017
Publication title -
journal of biomedical materials research part b: applied biomaterials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.665
H-Index - 108
eISSN - 1552-4981
pISSN - 1552-4973
DOI - 10.1002/jbm.b.33585
Subject(s) - vascular smooth muscle , intimal hyperplasia , phenotype , cancer research , mural cell , microbiology and biotechnology , cell growth , neointima , hyperplasia , cell , medicine , chemistry , biology , smooth muscle , biochemistry , restenosis , stent , gene
Intimal hyperplasia (IH) is the cause of clinical failure in patients with vascular transplants and intravascular stents. The proliferation and phenotype switching of vascular smooth muscle cells (VSMCs) play important roles in IH. Inhibiting the proliferation of VSMCs and maintaining the differentiated phenotype of VSMCs is one way to reduce IH. In this article, 5‐aminoimidazole‐4‐carboxamide 1‐β‐D‐ribofuranoside (AICAR) was used in experiments after drug screening. We found that the metabolism, autophagy, and differentiation of VSMCs were enhanced which were important to the normal function of VSMCs, but the secretion of VSMCs was reduced after AICAR treatment. AICAR induces G1 phase arrest and inhibits the proliferation of VSMCs using the MTT and EdU assays and cell cycle analysis. Then, the rat carotid artery vessel transplantation model was used to evaluate the function of AICAR in vivo . AICAR‐modified tissue‐engineered blood vessels (TEBVs) had a higher patency rate and less IH than the control TEBVs. In conclusion, AICAR can improve the normal function of VSMCs by increasing the metabolism and autophagy of VSMCs but inhibit the proliferation, paracrine, and phenotypes switching of VSMCs, further contribute the reducing of IH in TEBVs. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 105B: 744–752, 2017.