In vitro stimulation of articular chondrocyte mRNA and extracellular matrix synthesis by hydrostatic pressure

1996 ◽  
Vol 14 (1) ◽  
pp. 53-60 ◽  
Author(s):  
R. Lane Smith ◽  
S. F. Rusk ◽  
B. E. Ellison ◽  
P. Wessells ◽  
K. Tsuchiya ◽  
...  
2001 ◽  
Vol 16 (3) ◽  
pp. 500-505 ◽  
Author(s):  
Alessia Fornoni ◽  
Flavia Cornacchia ◽  
Guy A. Howard ◽  
Bernard A. Roos ◽  
Gary E. Striker ◽  
...  

1984 ◽  
Vol 119 (3) ◽  
pp. 359-365 ◽  
Author(s):  
M. F. Harmand ◽  
M. Thomasset ◽  
F. Rouais ◽  
D. Ducassou

Author(s):  
Najmuddin J. Gunja ◽  
Kyriacos A. Athanasiou

Cartilage explant studies have shown that mechanical stimuli increase extracellular matrix (ECM) expression and synthesis in vitro [1]. The use of hydrostatic pressure (HP), as a loading regimen, is of particular interest as it causes no cellular deformation. This may be useful in tissue engineering studies where scaffolds with limited mechanical integrity need to withstand intermittent loading conditions. Studies investigating the effect of HP on 3-D cultures of chondrocytes have met with modest success [2, 3]; however literature on meniscal fibrochondrocytes is lacking.


1979 ◽  
Vol 83 (2) ◽  
pp. 219-227 ◽  
Author(s):  
D. J. HILL

The actions of rat plasma somatomedin activity dependent on growth hormone were investigated in vitro on separated zones of cartilage from the calf costochondral junction. Plasma somatomedin maximally stimulated the uptake of [3H]thymidine into cartilage cells of the proliferating region. Cartilage deeper in the growth plate possessed the highest uptake of [35S]sulphate which was also stimulated by somatomedin. Somatomedin, therefore, appears to promote both cell replication and matrix synthesis throughout the growth plate cartilage although the two processes were greatest in different cartilage regions. Growth hormone or tri-iodothyronine did not directly alter the uptake of either isotope into the growth plate cartilage.


Cartilage ◽  
2017 ◽  
Vol 9 (2) ◽  
pp. 192-201 ◽  
Author(s):  
Takahiro Ogura ◽  
Akihiro Tsuchiya ◽  
Tom Minas ◽  
Shuichi Mizuno

Objective The effects of hydrostatic pressure (HP) on the matrix synthesis by human articular chondrocytes have been reported elsewhere. In order to optimize the production of extracellular matrix, we aimed to clarify the effects of repetitive HP on metabolic function by human articular chondrocytes. Design The human articular chondrocytes were expanded and embedded within a collagen gel/sponge scaffold. We incubated these constructs with and without HP followed by atmospheric pressure (AP) and repeated the second HP followed by AP over 14 days. Genomic, biochemical, and histological evaluation were performed to compare the effects of each regimen on the constructs. Results The gene expressions of collagen type II and aggrecan core protein were significantly upregulated with repetitive HP regimens compared with a single HP or AP by 14 days ( P < 0.01 or 0.05). Matrix metalloptoteinase-13 (MMP-13) in AP was upregulated significantly compared to other HP regimens at day 14 ( P < 0.01). No significant difference was observed in tissue inhibitor of metalloproteinases-II. Immunohistology demonstrated that application of HP (both repetitive and single) promoted the accumulation of specific extracellular matrix and reduced a MMP-13. A single regimen of HP followed by AP significantly increased the amount of sulfated glycosaminoglycan than that of the AP, whereas repetitive HP remained similar level of that of the AP. Conclusions Repetitive HP had a greater effect on anabolic activity by chondrocytes than a single HP regimen, which will be advantageous for producing a matrix-rich cell construct.


2012 ◽  
Vol 26 (9) ◽  
pp. 1385-1392 ◽  
Author(s):  
Lei Zhang ◽  
Xuan Zhang ◽  
Kui-Feng Li ◽  
Dong-Xiao Li ◽  
Yu-Mei Xiao ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Liang Tan ◽  
Yifang Xie ◽  
Ye Yuan ◽  
Kai Hu

The role of lncRNA growth arrest specific 5 (GAS5) in degenerative nucleus pulposus cell (NPC) apoptosis has been reported, but the mechanism of GAS5 in extracellular matrix (ECM) synthesis in intervertebral disc degeneration (IDD) remains unknown. We aimed to investigate the mechanism of GAS5 in ECM synthesis in degenerative NPCs. GAS5 expression was measured in degenerative NPCs (CP-H170) and normal NPCs (CP-H097). siRNA-mediated GAS5 knockdown was transfected to NPCs to detect cell viability and the expression of ECM-related genes (Collagen II, aggrecan, Collagen I, and MMP-3). Subcellular localization of GAS5 was analyzed. The downstream gene and pathway of GAS5 in degenerative NPCs were explored. As our results indicated, lncRNA GAS5 was upregulated in degenerative NPCs. Silencing GAS5 improved the viability of degenerative NPCs and increased ECM synthesis. GAS5 was mainly located in the cytoplasm of NPCs. LncRNA GAS5 sponged miR-26a-5p to regulate PTEN. Overexpression of miR-26a-5p promoted ECM synthesis in degenerative NPCs. Akt inhibitor LY294002 reversed the promotion of silencing GAS5 on ECM synthesis of degenerative NPCs. In conclusion, lncRNA GAS5 sponged miR-26a-5p to upregulate PTEN and inhibit the PI3K/Akt pathway, thus inhibiting ECM synthesis of degenerative NPCs.


Author(s):  
Yi Zhong ◽  
Arnold I Caplan ◽  
Jean F. Welter ◽  
Harihara Baskaran

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