- Tytuł:
- Excessive tensile strain induced the change in chondrocyte phenot
- Autorzy:
-
Zhong, D.
Chen, X.
Luo, Z.-P. - Powiązania:
- https://bibliotekanauki.pl/articles/306533.pdf
- Data publikacji:
- 2018
- Wydawca:
- Politechnika Wrocławska. Oficyna Wydawnicza Politechniki Wrocławskiej
- Tematy:
-
osteoartroza
fenotyp
chondrocyt
osteoarthritis
phenotype
chondrocytes
tensile strain - Opis:
- Chondrocyte extracellular matrix type II collagen and proteoglycans ensure an important compression-bearing structure in synovial joint. However, much more type I collagen is generated in osteoarthritis, which implies the presence of abnormal tensile strain in cartilage. We hypothesize that tensile stress influences chondrocyte phenotype at the cellular level, leading to potential osteoarthritis. Methods: Chondrocytes were stimulated with cyclic excessive tensile (10%) or mild tensile or compressive strain (5%) at 0.5 Hz, 3 h per day for 3 days. Chondrocyte morphology and matrix proteoglycans level was separately determined by Rhodamine phalloidin and toluidine blue staining. The expression of cartilage marker molecules was measured using quantitative reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assays. Results: Chondrocytes demonstrated significant fibroblastic morphology, reduced proliferation and increased apoptosis following exposure to 10% tensile strain. The 10% tensile strain group induced the lowest matrix proteoglycans level. It observably reduced the expression of COL2A1, Acan and SOX9, and increased COL1A1 expression level. The 5% tensile (5% compression) group, maintained the chondrocyte phenotype. Conclusions: The findings identified the effects of different magnitudes of tensile stress on chondrocyte phenotype compared to compressive strain. Further studies on cartilage biomechanical micro-environment might benefit from this study.
- Źródło:
-
Acta of Bioengineering and Biomechanics; 2018, 20, 2; 3-10
1509-409X
2450-6303 - Pojawia się w:
- Acta of Bioengineering and Biomechanics
- Dostawca treści:
- Biblioteka Nauki
Artykuł