Adipocyte in vascular wall can induce the rupture of abdominal aortic aneurysm

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作者
Hirona Kugo
Nobuhiro Zaima
Hiroki Tanaka
Youhei Mouri
Kenichi Yanagimoto
Kohsuke Hayamizu
Keisuke Hashimoto
Takeshi Sasaki
Masaki Sano
Tatsuro Yata
Tetsumei Urano
Mitsutoshi Setou
Naoki Unno
Tatsuya Moriyama
机构
[1] Graduate School of Agriculture,Department of Applied Biological Chemistry
[2] Kindai University,Department of Medical Physiology
[3] 204-3327 Nakamachi,Department of Anatomy and Neuroscience
[4] Hamamatsu University School of Medicine,Division of Vascular Surgery, Second Department of Surgery
[5] Human Life Science R&D Center,International Mass Imaging Center Department of Cellular and Molecular Anatomy and Preeminent Medical Photonics Education & Research Center Department of Systems Molecular Anatomy
[6] Nippon Suisan Kaisha,Department of Anatomy
[7] Ltd.,Division of Neural Systematics
[8] General Health Medical Center,undefined
[9] Yokohama University of Pharmacy,undefined
[10] Hamamatsu University School of Medicine,undefined
[11] Hamamatsu University School of Medicine,undefined
[12] Hamamatsu University School of Medicine,undefined
[13] 1-20-1 Handayama,undefined
[14] Higashi-ku,undefined
[15] Hamamatsu,undefined
[16] The university of Hong Kong,undefined
[17] 6/F,undefined
[18] National Institute for Physiological Sciences,undefined
来源
Scientific Reports | / 6卷
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摘要
Abdominal aortic aneurysm (AAA) is a vascular disease involving the gradual dilation of the abdominal aorta. It has been reported that development of AAA is associated with inflammation of the vascular wall; however, the mechanism of AAA rupture is not fully understood. In this study, we investigated the mechanism underlying AAA rupture using a hypoperfusion-induced animal model. We found that the administration of triolein increased the AAA rupture rate in the animal model and that the number of adipocytes was increased in ruptured vascular walls compared to non-ruptured walls. In the ruptured group, macrophage infiltration and the protein levels of matrix metalloproteinases 2 and 9 were increased in the areas around adipocytes, while collagen-positive areas were decreased in the areas with adipocytes compared to those without adipocytes. The administration of fish oil, which suppresses adipocyte hypertrophy, decreased the number and size of adipocytes, as well as decreased the risk of AAA rupture ratio by 0.23 compared to the triolein administered group. In human AAA samples, the amount of triglyceride in the adventitia was correlated with the diameter of the AAA. These results suggest that AAA rupture is related to the abnormal appearance of adipocytes in the vascular wall.
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