Phenotype stability, expansion potential, and senescence of embryonic tendon cells in vitro

Author(s):  
Phong K. Nguyen ◽  
Feiyang Deng ◽  
Sereen Assi ◽  
Paolo Paco ◽  
Spencer Fink ◽  
...  
Rheumatology ◽  
2014 ◽  
Vol 54 (2) ◽  
pp. 318-323 ◽  
Author(s):  
R. Mousavizadeh ◽  
L. Backman ◽  
R. G. McCormack ◽  
A. Scott

2007 ◽  
Vol 32 (3) ◽  
pp. 243-253 ◽  
Author(s):  
S. Lim ◽  
M. A. Hossain ◽  
J. Park ◽  
S. H. Choi ◽  
G. Kim

1977 ◽  
Vol 164 (3) ◽  
pp. 533-539 ◽  
Author(s):  
A Oikarinen

Collagen synthesis and the activities of prolyl hydroxylase, lysyl hydroxylase, collagen galactosyltransferase and collagen glucosyltransferase were studied in isolated chick-embryo tendon cells after the administration of cortisol acetate to the chick embryos. When the steroid was injected 1 day before isolation of the tendon cells, collagen synthesis was decreased, even though the enzyme activities were not changed. When cortisol acetate was given as repeated injections over a period of 4 days, both collagen synthesis and the enzyme activities decreased. The hydroxylase activities decreased even more than the two collagen glycosyltransferase activities, both in isolated cells and in whole chick embryos. The amount of prolyl hydroxylase protein diminished to the same extent as the enzyme activity, indicating that cortisol acetate inhibits enzyme synthesis. The inhibitory effect of cortisol acetate on collagen synthesis and on the enzyme activities was partially reversible in 3 days. Total protein synthesis was completely restored within this time. Only massive doses of cortisol acetate inhibited collagen synthesis in vitro. Additional experiments indicated that cortisol acetate did not decrease the rate of the enzyme reactions when added directly to the enzyme incubation mixtures. The results suggest that cortisol acetate decreases collagen synthesis both by its direct effect on collagen polypeptide-chain synthesis and by decreasing the activities of enzymes involved in post-translational modifications.


2010 ◽  
Vol 28 (8) ◽  
pp. 1078-1083 ◽  
Author(s):  
Kaori Sugioka ◽  
Koichi Nakagawa ◽  
Ryo Murata ◽  
Nobuyasu Ochiai ◽  
Takahisa Sasho ◽  
...  

2008 ◽  
Vol 21 (04) ◽  
pp. 337-342 ◽  
Author(s):  
M. A. Hossain ◽  
J. Park ◽  
S. H. Choi ◽  
G. Kim

SummaryDexamethasone (Dexa) has been commonly used in humans and domestic animals, particularly in the treatment of tendon injuries and cartilage degeneration. However, it is often associated with tendon rupture and impaired tendon and cartilage healing. In the present study, we investigated Dexa’s in vitro effects on the growth of cell proliferation and the induction of apoptosis in canine Achilles tendon cells and chondrocytes. Cell proliferation after treatment with Dexa for two to six days was quantified by a 2,3-bis{2-methoxy- 4-nitro-5-sulfophenyl}-2H-tetrazolium-5-carboxyanilide inner salt assay (XTT). The results showed that Dexa could inhibit the proliferation of tendon cells and chondrocytes at increasing concentrations (0.1–50 μg/ml) compared with untreated cells. Cell apoptosis was induced by Dexa, as evidenced by the typical nuclear apoptosis using Hoechst 33258 staining. Dexa increased the apoptosis of canine tendon cells and chondrocytes in a time-dependent manner. In canine tendon cells and chondrocytes that were treated with 25 and 50 μg/ml concentration of Dexa, the number of condensed apoptotic nuclei was significantly increased. In addition, culturing with Dexa and the glucocorticoid receptor blocker, mifepristone, significantly arrested apoptosis of tendon cells and chondrocytes. Based on our in vitro data, we hypothesized that in vivo treatment with glucocorticoids may diminish the proliferation of tendon and cartilage cells by increasing apoptosis and suppressing the proliferation. Our findings suggest that Dexa could be used with caution in dogs with articular or tendon problems.


1996 ◽  
Vol 10 (6) ◽  
pp. 743-754 ◽  
Author(s):  
G. Kempka ◽  
H.J. Ahr ◽  
W. Rüther ◽  
G. Schlüter
Keyword(s):  

2002 ◽  
Vol 20 (1) ◽  
pp. 36-39 ◽  
Author(s):  
Joanne Archambault ◽  
Mari Tsuzaki ◽  
Walter Herzog ◽  
Albert J. Banes

1999 ◽  
Vol 24 (6) ◽  
pp. 658-661 ◽  
Author(s):  
C. E. EVANS ◽  
G. C. LEES ◽  
I. A. TRAIL

The in vitro cytotoxicity of four cyanoacrylate adhesives was tested using cultures of cells derived from human tendons. All four were found to be cytotoxic, even at concentrations as low as 1.7%, over the experimental period of up to 18 weeks. This study shows that such adhesives in their present state may not be suitable for re-joining cut tendons as their initial and long-term toxicity may hinder the slow healing process of tendons.


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