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Highly Dispersed Fullerenols Hamper Osteoclast Ruffled Border Formation by Perturbing Ca2+ Bundles
Small ( IF 13.0 ) Pub Date : 2018-10-17 , DOI: 10.1002/smll.201802549 Weihong Gu 1, 2 , Kui Chen 1, 2 , Xiaoyi Zhao 2, 3 , Huan Geng 4 , Juan Li 1 , Yanxia Qin 1 , Xue Bai 1, 2 , Ya-Nan Chang 1 , Shibo Xia 1, 2 , Jiaxin Zhang 1, 2 , Sihan Ma 1 , Zhonghua Wu 3 , Gengyan Xing 4 , Gengmei Xing 1
Small ( IF 13.0 ) Pub Date : 2018-10-17 , DOI: 10.1002/smll.201802549 Weihong Gu 1, 2 , Kui Chen 1, 2 , Xiaoyi Zhao 2, 3 , Huan Geng 4 , Juan Li 1 , Yanxia Qin 1 , Xue Bai 1, 2 , Ya-Nan Chang 1 , Shibo Xia 1, 2 , Jiaxin Zhang 1, 2 , Sihan Ma 1 , Zhonghua Wu 3 , Gengyan Xing 4 , Gengmei Xing 1
Affiliation
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Osteoporosis, a common and serious bone disorder affecting aged people and postmenopausal women, is characterized by osteoclast overactivity. One therapeutic strategy is suppressing the bone resorption function of hyperactive osteoclasts, but there is no effective drug in clinical practice so far. Herein, it is demonstrated that fullerenols suppress the bone resorption of osteoclasts by inhibiting ruffled borders (RBs) formation. The RBs formation, which is supported by well‐aligned actin bundles (B‐actins), is a critical event for osteoclast bone resorption. To facilitate this function, osteoclast RBs dynamics is regulated by variable microenvironments to bundle F‐actins, protrude cell membrane, and so on. B‐actin perturbation by fullerenols is determined here, offering an opportunity to regulate osteoclast function by destroying RBs. In vivo, the therapeutic effect of fullerenols on overactive osteoclasts is confirmed in a mouse model of lipopolysaccharide‐induced bone erosion. Collectively, the findings suggest that fullerenols adhere to F‐actin surfaces and inhibit RBs formation in osteoclasts, mainly through hampering Ca2+ from bundling F‐actins, and this is likely due to the stereo‐hindrance effect caused by adherent fullerenols.
中文翻译：
高度分散的富勒烯醇会干扰Ca2 +束，从而阻碍破骨细胞皱纹形成边界。
骨质疏松症是一种影响老年人和绝经后妇女的常见且严重的骨骼疾病，其特征是破骨细胞过度活跃。一种治疗策略是抑制过度活跃的破骨细胞的骨吸收功能，但是迄今为止在临床实践中没有有效的药物。在此，证明了富勒烯醇通过抑制褶皱边界（RBs）的形成来抑制破骨细胞的骨吸收。RBs的形成受到良好排列的肌动蛋白束（B-actins）的支持，是破骨细胞骨吸收的关键事件。为促进此功能，破骨细胞RBs动力学受可变的微环境调节，以束缚F-肌动蛋白，突出细胞膜等。此处确定了富勒烯醇对B-肌动蛋白的扰动，从而提供了通过破坏RB来调节破骨细胞功能的机会。体内，在脂多糖诱导的骨侵蚀的小鼠模型中证实了富勒烯醇对过度活跃的破骨细胞的治疗作用。总体而言，研究结果表明，富勒烯醇粘附于F-肌动蛋白表面并抑制破骨细胞中的RBs形成，主要是通过阻碍Ca的形成。捆绑F-肌动蛋白2+，这可能是由于粘附的富勒烯醇引起的立体阻碍效应。
更新日期：2018-10-17
中文翻译：
高度分散的富勒烯醇会干扰Ca2 +束，从而阻碍破骨细胞皱纹形成边界。
骨质疏松症是一种影响老年人和绝经后妇女的常见且严重的骨骼疾病，其特征是破骨细胞过度活跃。一种治疗策略是抑制过度活跃的破骨细胞的骨吸收功能，但是迄今为止在临床实践中没有有效的药物。在此，证明了富勒烯醇通过抑制褶皱边界（RBs）的形成来抑制破骨细胞的骨吸收。RBs的形成受到良好排列的肌动蛋白束（B-actins）的支持，是破骨细胞骨吸收的关键事件。为促进此功能，破骨细胞RBs动力学受可变的微环境调节，以束缚F-肌动蛋白，突出细胞膜等。此处确定了富勒烯醇对B-肌动蛋白的扰动，从而提供了通过破坏RB来调节破骨细胞功能的机会。体内，在脂多糖诱导的骨侵蚀的小鼠模型中证实了富勒烯醇对过度活跃的破骨细胞的治疗作用。总体而言，研究结果表明，富勒烯醇粘附于F-肌动蛋白表面并抑制破骨细胞中的RBs形成，主要是通过阻碍Ca的形成。捆绑F-肌动蛋白2+，这可能是由于粘附的富勒烯醇引起的立体阻碍效应。
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