Accumulation of advanced oxidation protein products promotes age-related decline of type H vessels in bone.

Kai Zhao, Guo-Zheng Zhu, Hong-Zhou Li, Jia-Wen Gao, Chen Tu, Di-Zheng Wu, Yu-Sheng Huang, Dong Han, Xing-Yu Chen, Long-Yan Wu, Zhao-Ming Zhong
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Abstract

Type H vessels have been proven to couple angiogenesis and osteogenesis. The decline of type H vessels contributes to bone loss in the aging process. Aging is accompanied by the accumulation of advanced oxidation protein products (AOPPs). However, whether AOPP accumulation is involved in age-related decline of type H vessels is unclear. Here, we show that the increase of AOPP levels in plasma and bone were correlated with the decline of type H vessels and loss of bone mass in old mice. Exposure of microvascular endothelial cells to AOPPs significantly inhibited cell proliferation, migration, and tube formation, increased NADPH oxidase activity and excessive reactive oxygen species generation, upregulated the expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1, and eventually impaired angiogenesis, which was alleviated by redox modulator N-acetylcysteine and NADPH oxidase inhibitor apocynin. Furthermore, reduced AOPP accumulation by NAC treatment was able to alleviate significantly the decline of type H vessels, bone mass loss and deterioration of bone microstructure in old mice. Collectively, these findings suggest that AOPPs accumulation contributes to the decline of type H vessels in the aging process, and illuminate a novel potential mechanism underlying age-related bone loss.

高级氧化蛋白产物的积累会促进骨骼中 H 型血管与年龄相关的衰退。
H 型血管已被证明与血管生成和骨生成密切相关。在衰老过程中,H 型血管的衰退会导致骨质流失。衰老伴随着高级氧化蛋白产物(AOPPs)的积累。然而,AOPP 的积累是否参与了与年龄相关的 H 型血管衰退还不清楚。在这里,我们发现血浆和骨骼中 AOPP 水平的增加与老龄小鼠 H 型血管的衰退和骨量的损失有关。微血管内皮细胞暴露于 AOPPs 会显著抑制细胞增殖、迁移和管形成,增加 NADPH 氧化酶活性和过量活性氧的生成,上调血管细胞粘附分子-1 和细胞间粘附分子-1 的表达,并最终阻碍血管生成,而氧化还原调节剂 N-乙酰半胱氨酸和 NADPH 氧化酶抑制剂阿朴西宁可缓解这种情况。此外,通过 NAC 处理减少 AOPP 的积累能够显著缓解老龄小鼠 H 型血管的衰退、骨量减少和骨微结构的恶化。总之,这些研究结果表明,AOPPs 的积累是导致 H 型血管在衰老过程中衰退的原因之一,并揭示了与年龄相关的骨质流失的一种新的潜在机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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