Meniscus is a semilunar fibrocartilaginous tissue, serving important roles in load buffering, stability, lubrication, proprioception, and nutrition of the knee joint. The degeneration and damage of meniscus has been proved to be a risk factor of knee osteoarthritis. Mechanical stimulus is a critical factor of the development, maintenance and repair of the meniscus fibrochondrocytes. However, the mechanism of the mechano-transduction process remains elusive. Here we reported that cyclic hydrostatic compress force (CHCF) treatment promotes proliferation and inhibits apoptosis of the isolated primary meniscus fibrochondrocytes (PMFs), via upregulating the expression level of integrin ?5ß1. Consequently, increased phosphorylated-ERK1/2 and phosphorylated-PI3K, and decreased caspase-3 were detected. These effects of CHCF treatment can be abolished by integrin ?5ß1 inhibitor or specific siRNA transfection. These data indicate that CHCF regulates apoptosis of PMFs via integrin ?5ß1-FAK-PI3K/ERK pathway, which may be an important candidate approach during meniscus degeneration.
- MeSH
- Apoptosis physiology drug effects MeSH
- Mechanotransduction, Cellular physiology MeSH
- Chondrocytes metabolism drug effects MeSH
- Fibroblasts metabolism drug effects MeSH
- Hydrostatic Pressure MeSH
- Integrin alpha5beta1 antagonists & inhibitors metabolism MeSH
- Rats MeSH
- Cells, Cultured MeSH
- RNA, Small Interfering administration & dosage MeSH
- Meniscus cytology metabolism MeSH
- Compressive Strength physiology MeSH
- Rats, Sprague-Dawley MeSH
- Cell Proliferation physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- MeSH
- Bacterial Adhesion immunology drug effects MeSH
- Cytochalasin D pharmacology MeSH
- Epithelial Cells immunology MeSH
- Fibronectins immunology MeSH
- Research Support as Topic MeSH
- Genistein pharmacology MeSH
- Integrin alpha5beta1 analysis immunology MeSH
- Pseudomonas aeruginosa immunology pathogenicity MeSH
- In Vitro Techniques MeSH
