Cyclic hydrostatic compress force regulates apoptosis of meniscus fibrochondrocytes via integrin alpha5beta1
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
31177794
DOI
10.33549/physiolres.934088
PII: 934088
Knihovny.cz E-resources
- MeSH
- Apoptosis drug effects physiology MeSH
- Mechanotransduction, Cellular physiology MeSH
- Chondrocytes drug effects metabolism MeSH
- Fibroblasts drug effects metabolism 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
- Names of Substances
- Integrin alpha5beta1 MeSH
- RNA, Small Interfering MeSH
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.
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