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关节软骨碎片通过上调膜型基质金属蛋白酶 1 促进软骨细胞迁移。

Articular Cartilage Fragmentation Improves Chondrocyte Migration by Upregulating Membrane Type 1 Matrix Metalloprotease.

机构信息

Department of Orthopaedics, the First Affiliated Hospital of University of South China, Hengyang, Hunan, China.

Guangdong Hospital of Traditional Chinese Medicine, Zhuhai, Guangdong, China.

出版信息

Cartilage. 2021 Dec;13(2_suppl):1054S-1063S. doi: 10.1177/19476035211035435. Epub 2021 Oct 15.

Abstract

OBJECTIVE

This study was undertaken to elucidate the mechanism of improved chondrocyte migration after juvenile articular cartilage fragmentation.

DESIGN

organ culture with rabbit cartilage fragments and cell culture with rabbit chondrocytes were performed. In part A, minced juvenile cartilage fragments (0.5 × 0.5 × 0.5 mm) from rabbits, planted in gelatin sponge and fibrin glue, were cultured for 2, 4, or 6 weeks and compared with the cartilage chunks (4 × 4 × 1 mm) and membrane type 1 matrix metalloprotease (MT1-MMP) inhibitor groups. Chondrocyte outgrowth was evaluated on histology and confocal laser scanning microscopy. MT1-MMP expression was compared between the cartilage fragment group and the cartilage chunks group. In part B, articular chondrocytes were harvested from juvenile rabbits, MT1-MMP was transfected into the cells, and cell migration was evaluated using the Transwell and wound healing tests.

RESULTS

The histology and confocal microscopy results revealed that cell accumulation occurred at the edge of cartilage fragments, and outgrowth was better in the cartilage fragment group than those in the cartilage chunks group. Similar results were observed for MT1-MMP expression. After MT1-MMP inhibition, cells did not accumulate at the edge of the cartilage fragments, and chondrocyte outgrowth did not occur. Furthermore, overexpression of MT1-MMP enhanced the migration of articular chondrocytes.

CONCLUSIONS

Juvenile articular cartilage fragmentation improved chondrocyte migration by upregulating MT1-MMP.

摘要

目的

本研究旨在阐明幼年关节软骨碎裂后软骨细胞迁移改善的机制。

设计

进行了兔软骨碎片的器官培养和兔软骨细胞的细胞培养。在 A 部分中,将来自兔的碎幼年软骨碎片(0.5×0.5×0.5mm)种植在明胶海绵和纤维蛋白胶中,培养 2、4 或 6 周,并与软骨块(4×4×1mm)和膜型 1 基质金属蛋白酶(MT1-MMP)抑制剂组进行比较。通过组织学和共聚焦激光扫描显微镜评估软骨细胞的生长。比较软骨碎片组和软骨块组之间的 MT1-MMP 表达。在 B 部分中,从幼年兔中收获关节软骨细胞,将 MT1-MMP 转染到细胞中,并使用 Transwell 和划痕愈合试验评估细胞迁移。

结果

组织学和共聚焦显微镜结果显示,细胞在软骨碎片边缘聚集,并且在软骨碎片组中,生长情况优于软骨块组。MT1-MMP 表达也观察到类似的结果。在 MT1-MMP 抑制后,细胞不会在软骨碎片的边缘聚集,并且软骨细胞的生长没有发生。此外,MT1-MMP 的过表达增强了关节软骨细胞的迁移。

结论

幼年关节软骨碎裂通过上调 MT1-MMP 来改善软骨细胞的迁移。

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