Aggravated restenosis and atherogenesis in ApoCIII transgenic mice but lack of protection in ApoCIII knockouts: the effect of authentic triglyceride-rich lipoproteins with and without ApoCIII
Author(s) -
Haibo Li,
Yingchun Han,
Rong Qi,
Yuhui Wang,
Xiaohong Zhang,
Maomao Yu,
Yin Tang,
Mengyu Wang,
Ya-Nan Shu,
Wei Huang,
Xinfeng Liu,
Brian Rodrigues,
Mei Han,
Chaojie Liu
Publication year - 2015
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvv192
Subject(s) - medicine , endocrinology , restenosis , apolipoprotein b , biology , ldl receptor , knockout mouse , lipoprotein , hypertriglyceridemia , receptor , triglyceride , cholesterol , stent
Previously, our group and others have demonstrated a causative relationship between severe hypertriglyceridaemia and atherogenesis in mice. Furthermore, clinical investigations have shown high levels of plasma Apolipoprotein C-III (ApoCIII) associated with hypertriglyceridaemia and even cardiovascular disease. However, it remains unclear whether ApoCIII affects restenosis in vivo, and whether such an effect is mediated by ApoCIII alone, or in combination with hypertriglyceridaemia. We sought to investigate ApoCIII in restenosis and clarify how smooth muscle cells (SMCs) respond to authentic triglyceride-rich lipoproteins (TRLs) with or without ApoCIII (TRLs ± ApoCIII).
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