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Overexpression of perilipin1 protects against atheroma progression in apolipoprotein E knockout mice

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Title: Overexpression of perilipin1 protects against atheroma progression in apolipoprotein E knockout mice
Authors: Yamamoto, Kohei Browse this author
Miyoshi, Hideaki Browse this author →KAKEN DB
Cho, Kyu Yong Browse this author
Nakamura, Akinobu Browse this author →KAKEN DB
Greenberg, Andrew S. Browse this author
Atsumi, Tatsuya Browse this author →KAKEN DB
Keywords: Perilipin1
PLIN1
Macrophage
Atherosclerosis
Issue Date: Feb-2018
Publisher: Elsevier
Journal Title: Atherosclerosis
Volume: 269
Start Page: 192
End Page: 196
Publisher DOI: 10.1016/j.atherosclerosis.2018.01.019
PMID: 29407594
Abstract: Background and aims: Perilipin1 (PLIN1), a lipid droplet-associated protein, plays an important role in the regulation of lipolysis and lipid storage in adipocytes. PLIN1 has recently been reported to be expressed in macrophages within atheroma plaques, suggesting PLIN1 may play a role in the accumulation of lipids at the arterial wall and in the development of atherosclerosis. To clarify the role of PLIN1 in the pathophysiology of atherosclerosis, we assessed the progression of atherosclerosis in PLIN1 transgenic mice (Plin1Tg). Methods: Plin1Tg were crossed with apolipoprotein E knockout mice (ApoeKO). C57BL/6J mice, ApoeKO and Plin1Tg/ApoeKO received a normal chow diet for 20 weeks. Body weight, gonadal fat mass and plasma lipid concentrations were measured. Aortas were collected for quantification of atheroma lesions and histological analysis by Oil Red O staining. Results: Body weight, gonadal adipose mass and plasma triglyceride concentrations were not significantly different among the three groups. In contrast, the atherosclerotic lesion area was significantly increased in ApoeKO (14.2 +/- 3.2%; p<.01) compared with C57BL/6J mice (3.3 +/- 1.2%) and Plin1Tg/ApoeKO (5.6 +/- 1.9%). Conclusions: Overexpressed PLIN1 in macrophages had a protected role against atheroma progression in ApoeKO in the absence of changes in gonadal fat mass or plasma lipid levels, presumably due to modification of the stability and/or inflammatory profile of macrophages.
Rights: http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article
URI: http://hdl.handle.net/2115/68843
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)

Submitter: 三好 秀明

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