...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Osteoarthritis and cartilage >Deficiency of tenascin-C delays articular cartilage repair in mice.
【24h】

Deficiency of tenascin-C delays articular cartilage repair in mice.

机译：肌腱蛋白-C的缺乏会延缓小鼠的关节软骨修复。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

OBJECTIVE: In human articular cartilage, tenascin-C (TN-C) expression decreases during maturation of chondrocytes, and almost disappears in adults; however, it reappears in damaged cartilage. To examine the effects of TN-C on cartilage degeneration and repair, we compared articular cartilage degeneration between wild-type (WT) and tenascin-C knockout mouse (TNKO) mice using a spontaneous osteoarthritis (OA) in aged joints and surgical OA model. In addition, we made full-thickness cartilage defects and compared the cartilage repair process between the two groups. METHODS: The surgical procedure to create degenerative OA model was performed by transecting the anterior cruciate ligament and medial collateral ligament. Full-thickness defects were created in the center of the femoral trochlea to evaluate cartilage repair. Sections of cartilage were stained with hematoxylin and eosin or safranin-O, and immunostaining for TN-C. The degrees of degeneration and repair were graded. RESULTS: In the WT surgical OA model, the articular cartilage was almost normal at 2 weeks, but safranin-O decreased staining at 4 weeks. In TNKO mice, safranin-O decreased staining at 2 weeks, and cartilage was injured intensely at 4 weeks. In the cartilage repair model, TN-C was expressed after 1 week, was strongly expressed in the upper layer of regenerated tissue after 3 weeks, and disappeared after 6 weeks. The defects were restored until 6 weeks in WT mice; however, defects in TNKO mice were filled with fibrous tissue with no cartilage-like tissue. CONCLUSIONS: This study revealed that cartilage repair in TNKO mice was significantly slower than that in WT mice and that the deficiency of TN-C progressed during cartilage degeneration.
机译：目的：在人软骨中，软骨细胞成熟过程中腱生蛋白C（TN-C）表达下降，而在成年人中几乎消失。但是，它会重新出现在受损的软骨中。为了检查TN-C对软骨变性和修复的影响，我们比较了老年关节和手术OA模型中使用自发性骨关节炎（OA）的野生型（WT）和腱生蛋白C基因敲除小鼠（TNKO）小鼠之间的关节软骨变性。此外，我们制作了全层软骨缺损，并比较了两组之间的软骨修复过程。方法：通过切除前交叉韧带和内侧副韧带来进行手术，以建立变性OA模型。在股骨滑车的中心产生了全层缺损，以评估软骨修复。软骨切片用苏木精和曙红或番红O-O染色，并对TN-C进行免疫染色。对退化和修复的程度进行分级。结果：在WT手术OA模型中，关节软骨在第2周时几乎是正常的，而番红O在第4周时减少了染色。在TNKO小鼠中，番红素O在2周时减少了染色，并且在4周时严重损伤了软骨。在软骨修复模型中，TN-C在1周后表达，在3周后在再生组织的上层强烈表达，并在6周后消失。在WT小鼠中，缺陷被恢复到6周。但是，TNKO小鼠的缺损中充满了没有软骨样组织的纤维组织。结论：这项研究表明，TNKO小鼠的软骨修复明显慢于WT小鼠，并且TN-C缺乏在软骨变性过程中发展。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号