期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 236, 期 8, 页码 5714-5724出版社
WILEY
DOI: 10.1002/jcp.30256
关键词
F‐ actin fibers; mechanobiology; mechanotransduction; nucleus; osteoprotegerin; periodontal disease; periodontal ligament fibroblasts
资金
- CPRIT [RR200043, RP170719]
- Center for Molecular Microbiology, University of Florida, Gainesville
The study found that in a mouse model of periodontal disease, periodontal ligament fibroblasts (PdLFs) exhibit rounded and disoriented nuclei, indicating reduced actomyosin tension. Inhibiting actomyosin contractility decreased levels of bone regulatory protein osteoprotegerin (OPG). Infection with periodontal bacteria did not replicate the observed nuclear rounding in vivo.
Periodontal ligament fibroblasts (PdLFs) are an elongated cell type in the periodontium with matrix and bone regulatory functions which become abnormal in periodontal disease (PD). Here we found that the normally elongated and oriented PdLF nucleus becomes rounded and loses orientation in a mouse model of PD. Using in vitro micropatterning of cultured primary PdLF cell shape, we show that PdLF elongation correlates with nuclear elongation and the presence of thicker, contractile F-actin fibers. The rounded nuclei in mouse PD models in vivo are, therefore, indicative of reduced actomyosin tension. Inhibiting actomyosin contractility by inhibiting myosin light chain kinase, Rho kinase or myosin ATPase activity, in cultured PdLFs each consistently reduced messenger RNA levels of bone regulatory protein osteoprotegerin (OPG). Infection of cultured PdLFs with two different types of periodontal bacteria (Porphyromonas gingivalis and Fusobacterium nucleatum) failed to recapitulate the observed nuclear rounding in vivo, upregulated nonmuscle myosin II phosphorylation and downregulated OPG. Collectively, our results add support to the hypothesis that PdLF contractility becomes decreased and contributes to disease progression in PD.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据