The Coordinated Interplay Between MMP13 and Pro-Migratory MMPs in Collective Cell Migration of Zebrafish Keratocytes

斑马鱼角质细胞集体迁移中 MMP13 与促迁移 MMP 的协同作用

阅读:2

Abstract

Collective cell migration (CCM) is a coordinated process involving cell-cell and cell-environment interactions occurring in many physiological systems, including development, wound healing, and metastasis. Using zebrafish keratocytes as a wound healing model provides a unique system to investigate the interplay of matrix metalloproteinases (MMPs) in CCM. MMPs play an important role in CCM as they generate bioactive molecules that regulate proliferation, differentiation, angiogenesis, apoptosis, and cell migration. Secreted as pro-enzymes, MMPs must be activated, frequently by another MMP. As a group, MMPs have been reported to have a pro-migratory role during CCM, yet our data reveal that one MMP, MMP13, is not pro-migratory. Treatment of keratocytes with recombinant MMP13 resulted in a dose-dependent decrease in migration, reduced MMP13 activity, and increased MMP9 mRNA expression. Treatment with an MMP13-specific inhibitor resulted in a dose-dependent increase in migration with no change in the rate of cellular proliferation, an increase in total MMP activity, and increased MMP2 mRNA expression. Similarly, inhibition of MMP14 also resulted in a significant, dose-dependent decrease in migration. However, MMP14 inhibition resulted in both an increase in MMP2 mRNA expression and a decrease in MMP9 mRNA expression. The increase in MMP2 and/or MMP9 activity was observed on gel zymography for both treatments. Our data support the hypothesis that MMP13 is anti-migratory while MMP2, MMP9 and MMP14 have a pro-migratory effect on zebrafish keratocytes. Taken together, our results outline a novel inhibitory role for MMP regulation of CCM that has implications for many other processes in multicellular organisms.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。