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骨保护素缺失对小鼠腹主动脉瘤形成过程中的中膜破坏和外膜纤维化有复杂影响。

Disruption of Osteoprotegerin has complex effects on medial destruction and adventitial fibrosis during mouse abdominal aortic aneurysm formation.

机构信息

Department of Cardiovascular Physiology and Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

出版信息

PLoS One. 2020 Jul 2;15(7):e0235553. doi: 10.1371/journal.pone.0235553. eCollection 2020.

DOI:10.1371/journal.pone.0235553
PMID:32614927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7331998/
Abstract

Aortic aneurysm refers to dilatation of the aorta due to loss of elasticity and degenerative weakening of its wall. A preventive role for osteoprotegerin (Opg) in the development of abdominal aortic aneurysm has been reported in the CaCl2-induced aneurysm model, whereas Opg was found to promote suprarenal aortic aneurysm in the AngII-induced ApoE knockout mouse aneurysm model. To determine whether there is a common underlying mechanism to explain the impact of Opg deficiency on the vascular structure of the two aneurysm models, we analyzed suprarenal aortic tissue of 6-month-old ApoE-/-Opg-/- mice after AngII infusion for 28 days. Less aortic dissection and aortic lumen dilatation, more adventitial thickening, and higher expression of collagen I and Trail were observed in ApoE-/-Opg-/- mice relative to ApoE-/-Opg+/+ mice. An accumulation of α-smooth muscle actin and vimentin double-positive myofibroblasts was noted in the thickened adventitia of ApoE-/-Opg-/- mice. Our results suggest that fibrotic remodeling of the aorta induced by myofibroblast accumulation might be an important pathological event which tends to limit AngII-induced aortic dilatation in ApoE -/-Opg-/- mice.

摘要

主动脉瘤是指由于主动脉壁弹性丧失和退行性变导致的主动脉扩张。在 CaCl2 诱导的动脉瘤模型中，已经报道了骨保护素（Opg）在腹主动脉瘤发生中的预防作用，而在 AngII 诱导的 ApoE 敲除小鼠动脉瘤模型中，Opg 被发现促进了肾上腹主动脉瘤的发生。为了确定 Opg 缺乏对两种动脉瘤模型的血管结构的影响是否存在共同的潜在机制，我们在 AngII 输注 28 天后分析了 6 个月大的 ApoE-/-Opg-/-小鼠的肾上腹主动脉组织。与 ApoE-/-Opg+/+小鼠相比，ApoE-/-Opg-/-小鼠的主动脉夹层较少，主动脉腔扩张较少，外膜较厚，胶原 I 和 Trail 的表达水平较高。在 ApoE-/-Opg-/-小鼠增厚的外膜中，观察到 α-平滑肌肌动蛋白和波形蛋白双阳性的肌成纤维细胞的积累。我们的结果表明，由肌成纤维细胞积累引起的主动脉纤维化重塑可能是一种重要的病理事件，它可能限制 ApoE-/-Opg-/-小鼠 AngII 诱导的主动脉扩张。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/f3f9a787c93b/pone.0235553.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/8df2b69f15c9/pone.0235553.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/e0e63433e1f7/pone.0235553.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/373d085c367f/pone.0235553.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/855c362ee9d6/pone.0235553.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/f3f9a787c93b/pone.0235553.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/8df2b69f15c9/pone.0235553.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/e0e63433e1f7/pone.0235553.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/373d085c367f/pone.0235553.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/855c362ee9d6/pone.0235553.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eba/7331998/f3f9a787c93b/pone.0235553.g005.jpg

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