Stromal cell-derived factor 1 regulates the actin organization of chondrocytes and chondrocyte hypertrophy.
Stromal cell-derived factor 1 regulates the actin organization of chondrocytes and chondrocyte hypertrophy.
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基质细胞衍生的因子1调节软骨细胞和软骨细胞肥大的肌动蛋白组织。
DOI：
10.1371/journal.pone.0037163
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Ito H
中科院分区：
文献类型：
--
作者：
Murata K;Kitaori T;Oishi S;Watanabe N;Yoshitomi H;Tanida S;Ishikawa M;Kasahara T;Shibuya H;Fujii N;Nagasawa T;Nakamura T;Ito H
基质细胞衍生因子 1 (SDF-1/CXCL12/PBSF) 在造血干细胞和间充质干细胞的生物学和生理功能中发挥着重要作用。这种趋化因子在胚胎发生过程中调节多个器官系统的形成。然而，它在骨骼发育中的作用仍不清楚。在这里，我们研究了 SDF-1 在软骨细胞分化中的作用。我们通过免疫组织化学分析证明，SDF-1蛋白在肋骨骨折新形成的软骨内愈伤组织以及正常小鼠胫骨生长板的肥大前和肥大软骨细胞中表达。使用SDF-1−/−小鼠胚胎，我们通过组织学观察发现，SDF-1−/−小鼠的整个肱骨总长度明显短于野生型小鼠，这主要是由于SDF-1−/−小鼠的肥厚区和钙化区较短。 SDF-1−/− 小鼠肱骨肥大软骨细胞的肌动蛋白细胞骨架显示出比野生型小鼠更少的 F-肌动蛋白和更圆的形状。来自 SDF-1−/− 小鼠的原代软骨细胞显示出伪足的形成增强和 F-肌动蛋白的损失。对野生型小鼠和SDF-1−/−小鼠的原代软骨细胞施用SDF-1促进了肌动蛋白应力纤维的形成。 SDF-1−/− 小鼠胚胎跖骨的器官培养显示生长延迟，通过外源性施用 SDF-1 可以恢复生长延迟。当向跖骨施用SDF-1恢复时，SDF-1−/−小鼠胚胎的跖骨和原代软骨细胞中X型胶原的mRNA表达下调。这些数据表明，SDF-1 通过介导软骨细胞肥大来调节肌动蛋白组织并刺激骨骼生长。
Stromal cell-derived factor 1 (SDF-1/CXCL12/PBSF) plays important roles in the biological and physiological functions of haematopoietic and mesenchymal stem cells. This chemokine regulates the formation of multiple organ systems during embryogenesis. However, its roles in skeletal development remain unclear. Here we investigated the roles of SDF-1 in chondrocyte differentiation. We demonstrated that SDF-1 protein was expressed at pre-hypertrophic and hypertrophic chondrocytes in the newly formed endochondral callus of rib fracture as well as in the growth plate of normal mouse tibia by immunohistochemical analysis. Using SDF-1−/− mouse embryo, we histologically showed that the total length of the whole humeri of SDF-1−/− mice was significantly shorter than that of wild-type mice, which was contributed mainly by shorter hypertrophic and calcified zones in SDF-1−/− mice. Actin cytoskeleton of hypertrophic chondrocytes in SDF-1−/− mouse humeri showed less F-actin and rounder shape than that of wild-type mice. Primary chondrocytes from SDF-1−/− mice showed the enhanced formation of philopodia and loss of F-actin. The administration of SDF-1 to primary chondrocytes of wild-type mice and SDF-1−/− mice promoted the formation of actin stress fibers. Organ culture of embryonic metatarsals from SDF-1−/− mice showed the growth delay, which was recovered by an exogenous administration of SDF-1. mRNA expression of type X collagen in metatarsals and in primary chondrocytes of SDF-1−/− mouse embryo was down-regulated while the administration of SDF-1 to metatarsals recovered. These data suggests that SDF-1 regulates the actin organization and stimulates bone growth by mediating chondrocyte hypertrophy.
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影响因子：
9.5
作者：
Ma, J;Ge, JB;Zou, YZ
通讯作者：
Zou, YZ
影响因子：
2.3
作者：
Kucia, M;Ratajczak, J;Ratajczak, MZ
通讯作者：
Ratajczak, MZ
影响因子：
10.5
作者：
Murakami, S;Balmes, G;de Crombrugghe, B
通讯作者：
de Crombrugghe, B
影响因子：
5.6
作者：
Grassi, F;Cristino, S;Lisignoli, G
通讯作者：
Lisignoli, G
影响因子：
5.2
作者：
Ji, JF;He, BP;Tay, SSW
通讯作者：
Tay, SSW