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Published on: September 26, 2018
Phospholipid transfer protein destabilizes mouse atherosclerotic plaque
Ke Zhang1, Xiaoling Liu1, Yang Yu1
1From The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Shandong University Qilu Hospital, Jinan, Shandong, People's Republic of China (K.Z., X.L., L.W., C.G., X.L., J.S., Y.Z., M.Z.); The Key Laboratory of Atherosclerosis in Universities of Shandong, Institute of Atherosclerosis, Taishan Medical University, Taian, Shandong, People's Republic of China (Y.Y., T.L., S.Q.); and Department of Cell Biology, State University of New York, Downstate Medical Center, New York (X.J.).
Phospholipid transfer protein (PLTP) impacts atherosclerotic plaque stability. Its deficiency improved plaque stability, while overexpression worsened it, highlighting PLTP
Area of Science:
- Cardiovascular Biology
- Atherosclerosis Research
Background:
- Phospholipid transfer protein (PLTP) is implicated in accelerating atherosclerosis development.
- Understanding PLTP's role in atherosclerotic plaque stability is crucial for therapeutic strategies.
Purpose of the Study:
- To investigate the specific role of PLTP in modulating atherosclerotic plaque stability.
- To elucidate the molecular mechanisms underlying PLTP's effects on plaque progression.
Main Methods:
- Generation and analysis of apolipoprotein E and PLTP double-knockout mice.
- Assessment of atherosclerotic plaque characteristics, including lesion size, immune cell infiltration, and fibrous content.
- Investigation of PLTP overexpression effects using adenovirus mediation in mouse models.
Main Results:
- PLTP deficiency significantly reduced atherosclerotic lesion size, monocyte/macrophage infiltration, and macrophage apoptosis.
- PLTP deficiency increased fibrous content in plaques, indicating enhanced stability.
- PLTP overexpression promoted reactive oxygen species accumulation, inflammatory cytokine production, and receptor-interacting protein 3 recruitment in macrophages, exacerbating atherogenesis.
Conclusions:
- PLTP plays a significant role in regulating atherosclerotic plaque stability.
- The receptor-interacting protein 3-reactive oxygen species signaling pathway is implicated in PLTP-mediated atherogenesis.
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