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Wnt/β-连环蛋白信号通路抑制肌腱衍生细胞中Scx、Mkx和Tnmd的表达。

Wnt/β-catenin signaling suppresses expressions of Scx, Mkx, and Tnmd in tendon-derived cells.

作者信息

Kishimoto Yasuzumi, Ohkawara Bisei, Sakai Tadahiro, Ito Mikako, Masuda Akio, Ishiguro Naoki, Shukunami Chisa, Docheva Denitsa, Ohno Kinji

机构信息

Division of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Department of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

出版信息

PLoS One. 2017 Jul 27;12(7):e0182051. doi: 10.1371/journal.pone.0182051. eCollection 2017.

DOI:10.1371/journal.pone.0182051
PMID:28750046
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5531628/
Abstract

After tendon injuries, biomechanical properties of the injured tendon are not fully recovered in most cases. Modulation of signaling pathways, which are involved in tendon development and tendon repair, is one of attractive modalities to facilitate proper regeneration of the injured tendon. The roles of TGF-β signaling in tendon homeostasis and tendon development have been elucidated. In contrast, the roles of Wnt/β-catenin signaling in tendon remain mostly elusive. We found that the number of β-catenin-positive cells was increased at the injured site, suggesting involvement of Wnt/β-catenin signaling in tendon healing. Activation of Wnt/β-catenin signaling suppressed expressions of tenogenic genes of Scx, Mkx, and Tnmd in rat tendon-derived cells (TDCs) isolated from the Achilles tendons of 6-week old rats. Additionally, activation of Wnt/β-catenin reduced the amounts of Smad2 and Smad3, which are intracellular mediators for TGF-β signaling, and antagonized upregulation of Scx induced by TGF-β signaling in TDCs. We found that Wnt/β-catenin decreased Mkx and Tnmd expressions without suppressing Scx expression in Scx-programmed tendon progenitors. Our studies suggest that Wnt/β-catenin signaling is a repressor for tenogenic gene expressions.

摘要

肌腱损伤后，在大多数情况下，受损肌腱的生物力学特性无法完全恢复。调节参与肌腱发育和肌腱修复的信号通路，是促进受损肌腱正确再生的一种有吸引力的方式。TGF-β信号在肌腱稳态和肌腱发育中的作用已经阐明。相比之下，Wnt/β-连环蛋白信号在肌腱中的作用大多仍不清楚。我们发现，β-连环蛋白阳性细胞的数量在损伤部位增加，这表明Wnt/β-连环蛋白信号参与了肌腱愈合。Wnt/β-连环蛋白信号的激活抑制了从6周龄大鼠跟腱分离的大鼠肌腱来源细胞（TDCs）中肌腱生成基因Scx、Mkx和Tnmd 的表达。此外，Wnt/β-连环蛋白的激活减少了Smad2和Smad3的量，Smad2和Smad3是TGF-β信号的细胞内介质，并拮抗了TDCs中由TGF-β信号诱导的Scx上调。我们发现，Wnt/β-连环蛋白在Scx编程的肌腱祖细胞中降低了Mkx和Tnmd的表达，而没有抑制Scx的表达。我们的研究表明，Wnt/β-连环蛋白信号是肌腱生成基因表达的抑制因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/2eab1f09a506/pone.0182051.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/0d6d83e3660d/pone.0182051.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/a06ff56a96ce/pone.0182051.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/99099b6360a6/pone.0182051.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/7c6e26297496/pone.0182051.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/54caf71a27ae/pone.0182051.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/2eab1f09a506/pone.0182051.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/0d6d83e3660d/pone.0182051.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/a06ff56a96ce/pone.0182051.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/99099b6360a6/pone.0182051.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/7c6e26297496/pone.0182051.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/54caf71a27ae/pone.0182051.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf4a/5531628/2eab1f09a506/pone.0182051.g006.jpg

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