Suppr超能文献

母体高脂饮食通过 IRF8 介导的破骨细胞样巨噬细胞分化的表观遗传调控促进成年子代腹主动脉瘤扩张。

Maternal High-Fat Diet Promotes Abdominal Aortic Aneurysm Expansion in Adult Offspring by Epigenetic Regulation of IRF8-Mediated Osteoclast-like Macrophage Differentiation.

机构信息

Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Department of Regenerative Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

出版信息

Cells. 2021 Aug 27;10(9):2224. doi: 10.3390/cells10092224.

Abstract

Maternal high-fat diet (HFD) modulates vascular remodeling in adult offspring. Here, we investigated the impact of maternal HFD on abdominal aortic aneurysm (AAA) development. Female wild-type mice were fed an HFD or normal diet (ND). AAA was induced in eight-week-old pups using calcium chloride. Male offspring of HFD-fed dams (O-HFD) showed a significant enlargement in AAA compared with the offspring of ND-fed dams (O-ND). Positive-staining cells for tartrate-resistant acid phosphate (TRAP) and matrix metalloproteinase (MMP) activity were significantly increased in O-HFD. The pharmacological inhibition of osteoclastogenesis abolished the exaggerated AAA development in O-HFD. The in vitro tumor necrosis factor-α-induced osteoclast-like differentiation of bone marrow-derived macrophages showed a higher number of TRAP-positive cells and osteoclast-specific gene expressions in O-HFD. Consistent with an increased expression of nuclear factor of activated T cells 1 (NFATc1) in O-HFD, the nuclear protein expression of interferon regulatory factor 8 (IRF8), a transcriptional repressor, were much lower, with significantly increased H3K27me3 marks at the promoter region. The enhancer of zeste homolog 2 inhibitor treatment restored IRF8 expression, resulting in no difference in NFATc1 and TRAP expressions between the two groups. Our findings demonstrate that maternal HFD augments AAA expansion, accompanied by exaggerated osteoclast-like macrophage accumulation, suggesting the possibility of macrophage skewing via epigenetic reprogramming.

摘要

母体高脂肪饮食(HFD)可调节成年后代的血管重塑。在这里,我们研究了母体 HFD 对腹主动脉瘤(AAA)发展的影响。雌性野生型小鼠分别喂食 HFD 或正常饮食(ND)。使用氯化钙诱导 8 周大的幼鼠 AAA。与 ND 喂养的母鼠(O-ND)的后代相比,HFD 喂养的母鼠的雄性后代(O-HFD)的 AAA 明显增大。抗酒石酸酸性磷酸酶(TRAP)和基质金属蛋白酶(MMP)活性的阳性染色细胞在 O-HFD 中显著增加。破骨细胞生成的药理学抑制消除了 O-HFD 中 AAA 发育的夸大。体外肿瘤坏死因子-α诱导的骨髓来源巨噬细胞破骨细胞样分化显示 O-HFD 中 TRAP 阳性细胞和破骨细胞特异性基因表达增加。与 O-HFD 中核因子活化 T 细胞 1(NFATc1)的表达增加一致,干扰素调节因子 8(IRF8)的核蛋白表达要低得多,其启动子区域的 H3K27me3 标记明显增加。EZH2 抑制剂处理恢复了 IRF8 的表达,导致两组之间 NFATc1 和 TRAP 表达无差异。我们的研究结果表明,母体 HFD 增强了 AAA 的扩张,同时伴有破骨细胞样巨噬细胞的大量积累,提示通过表观遗传重编程发生巨噬细胞偏斜的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5873/8466477/148958dfe96e/cells-10-02224-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验