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Natural Killer T Cells Are Involved in Atherosclerotic Plaque Instability in Apolipoprotein-E Knockout Mice

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Title: Natural Killer T Cells Are Involved in Atherosclerotic Plaque Instability in Apolipoprotein-E Knockout Mice
Authors: Ohmura, Yoshinori Browse this author
Ishimori, Naoki Browse this author →KAKEN DB
Saito, Akimichi Browse this author
Yokota, Takashi Browse this author →KAKEN DB
Horii, Shunpei Browse this author
Tokuhara, Satoshi Browse this author
Iwabuchi, Kazuya Browse this author
Tsutsui, Hiroyuki Browse this author
Keywords: alpha-galactosylceramide
apolipoprotein E knockout mice
brachiocephalic artery
matrix metalloproteinase
natural killer T cells
plaque instability
Issue Date: Nov-2021
Publisher: MDPI
Journal Title: International Journal of Molecular Sciences
Volume: 22
Issue: 22
Start Page: 12451
Publisher DOI: 10.3390/ijms222212451
Abstract: The infiltration and activation of macrophages as well as lymphocytes within atherosclerotic lesion contribute to the pathogenesis of plaque rupture. We have demonstrated that invariant natural killer T (iNKT) cells, a unique subset of T lymphocytes that recognize glycolipid antigens, play a crucial role in atherogenesis. However, it remained unclear whether iNKT cells are also involved in plaque instability. Apolipoprotein E (apoE) knockout mice were fed a standard diet (SD) or a high-fat diet (HFD) for 8 weeks. Moreover, the SD- and the HFD-fed mice were divided into two groups according to the intraperitoneal injection of alpha-galactosylceramide (alpha GC) that specifically activates iNKT cells or phosphate-buffered saline alone (PBS). ApoE/J alpha 18 double knockout mice, which lack iNKT cells, were also fed an SD or HFD. Plaque instability was assessed at the brachiocephalic artery by the histological analysis. In the HFD group, alpha GC significantly enhanced iNKT cell infiltration and exacerbated atherosclerotic plaque instability, whereas the depletion of iNKT cells attenuated plaque instability compared to PBS-treated mice. Real-time PCR analyses in the aortic tissues showed that alpha GC administration significantly increased expressional levels of inflammatory genes such as IFN-gamma and MMP-2, while the depletion of iNKT cells attenuated these expression levels compared to those in the PBS-treated mice. Our findings suggested that iNKT cells are involved in the exacerbation of plaque instability via the activation of inflammatory cells and upregulation of MMP-2 in the vascular tissues.
Type: article
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

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