Influence of 17β-estradiol and insulin on type II collagen and protein synthesis of articular chondrocytes

Bone ◽  
2006 ◽  
Vol 39 (2) ◽  
pp. 310-317 ◽  
Author(s):  
Horst Claassen ◽  
Matthias Schlüter ◽  
Michael Schünke ◽  
Bodo Kurz
Keyword(s):  
Protein Synthesis ◽  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Type Ii ◽  
17Β Estradiol

scholarly journals Up-regulation of type II collagen gene by 17β-estradiol in articular chondrocytes involves Sp1/3, Sox-9, and estrogen receptor α

2014 ◽  
Vol 92 (11) ◽  
pp. 1179-1200 ◽  
Author(s):  
Laure Maneix ◽  
Aurélie Servent ◽  
Benoît Porée ◽  
David Ollitrault ◽  
Thomas Branly ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Estrogen Receptor Α ◽  
Collagen Gene ◽  
Type Ii ◽  
17Β Estradiol

scholarly journals Regulation of type II collagen expression by cyclin-dependent kinase 6, cyclin D1, and p21 in articular chondrocytes

IUBMB Life ◽  
2007 ◽  
Vol 59 (2) ◽  
pp. 90-98 ◽  
Author(s):  
Sang-Gu Hwang ◽  
Sung-Min Song ◽  
Jeong-Ran Kim ◽  
Chun-Shik Park ◽  
Woo-Keun Song ◽  
...  
Keyword(s):  
Cyclin D1 ◽  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Cyclin Dependent Kinase ◽  
Collagen Expression

SOX9 expression does not correlate with type II collagen expression in adult articular chondrocytes

2003 ◽  
Vol 22 (4) ◽  
pp. 363-372 ◽  
Author(s):  
Thomas Aigner ◽  
Pia Margarethe Gebhard ◽  
Erik Schmid ◽  
Brigitte Bau ◽  
Vincent Harley ◽  
...  
Keyword(s):  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Sox9 Expression ◽  
Collagen Expression

Facilitating In Vivo Articular Cartilage Repair by Tissue-Engineered Cartilage Grafts Produced From Auricular Chondrocytes

2017 ◽  
Vol 46 (3) ◽  
pp. 713-727 ◽  
Author(s):  
Chin-Chean Wong ◽  
Chih-Hwa Chen ◽  
Li-Hsuan Chiu ◽  
Yang-Hwei Tsuang ◽  
Meng-Yi Bai ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Articular Cartilage ◽  
Cartilage Repair ◽  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Articular Cartilage Repair ◽  
3 Dimensional ◽  
Cell Conversion

Background: Insufficient cell numbers still present a challenge for articular cartilage repair. Converting heterotopic auricular chondrocytes by extracellular matrix may be the solution. Hypothesis: Specific extracellular matrix may convert the phenotype of auricular chondrocytes toward articular cartilage for repair. Study Design: Controlled laboratory study. Methods: For in vitro study, rabbit auricular chondrocytes were cultured in monolayer for several passages until reaching status of dedifferentiation. Later, they were transferred to chondrogenic type II collagen (Col II)–coated plates for further cell conversion. Articular chondrogenic profiles, such as glycosaminoglycan deposition, articular chondrogenic gene, and protein expression, were evaluated after 14-day cultivation. Furthermore, 3-dimensional constructs were fabricated using Col II hydrogel-associated auricular chondrocytes, and their histological and biomechanical properties were analyzed. For in vivo study, focal osteochondral defects were created in the rabbit knee joints, and auricular Col II constructs were implanted for repair. Results: The auricular chondrocytes converted by a 2-step protocol expressed specific profiles of chondrogenic molecules associated with articular chondrocytes. The histological and biomechanical features of converted auricular chondrocytes became similar to those of articular chondrocytes when cultivated with Col II 3-dimensional scaffolds. In an in vivo animal model of osteochondral defects, the treated group (auricular Col II) showed better cartilage repair than did the control groups (sham, auricular cells, and Col II). Histological analyses revealed that cartilage repair was achieved in the treated groups with abundant type II collagen and glycosaminoglycans syntheses rather than elastin expression. Conclusion: The study confirmed the feasibility of applying heterotopic chondrocytes for cartilage repair via extracellular matrix–induced cell conversion. Clinical Relevance: This study proposes a feasible methodology to convert heterotopic auricular chondrocytes for articular cartilage repair, which may serve as potential alternative sources for cartilage repair.

Neutral proteinases from articular chondrocytes in culture. I. A latent collagenase that degrades human cartilage type II collagen

1981 ◽  
Vol 657 (2) ◽  
pp. 517-529 ◽  
Author(s):  
Charles J. Malemud ◽  
David P. Norby ◽  
Asher I. Sapolsky ◽  
Kunio Matsuta ◽  
David S. Howell ◽  
...  
Keyword(s):  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Human Cartilage

scholarly journals Microfilament modification by dihydrocytochalasin B causes retinoic acid-modulated chondrocytes to reexpress the differentiated collagen phenotype without a change in shape.

1988 ◽  
Vol 106 (1) ◽  
pp. 161-170 ◽  
Author(s):  
P D Benya ◽  
P D Brown ◽  
S R Padilla
Keyword(s):  
Retinoic Acid ◽  
Cell Shape ◽  
Articular Chondrocytes ◽  
Type Ii Collagen ◽  
Phenotypic Change ◽  
Type Iii Collagen ◽  
Type I ◽  
Type Ii ◽  
The Stability ◽  
Rabbit Articular Chondrocytes

Primary monolayers of rabbit articular chondrocytes synthesize high levels of type II collagen and proteoglycan. This capacity was used as a marker for the expression of the differentiated phenotype. Such cells were treated with 1 microgram/ml retinoic acid (RA) for 10 d to produce a modulated collagen phenotype devoid of type II and consisting of predominantly type I trimer and type III collagen. After transfer to secondary culture in the presence of RA, the stability of the RA-modulated phenotype was investigated by culture in the absence of RA. Little reexpression of type II collagen synthesis occurred in this period unless cultures were treated with 3 X 10(-6) M dihydrocytochalasin B to modify microfilament structures. Reexpression of the differentiated phenotype began between days 6-8 and was essentially complete by day 14. Substantial reexpression occurred by day 8 without a detectable increase in cell rounding. Colony formation, characteristic of primary chondrocytes, was infrequent even after reexpression was complete. These data suggest that the integrity of microfilament cytoskeletal structures can be a source of regulatory signals that mechanistically appear to be more proximal to phenotypic change than the overt changes in cell shape that accompany reexpression of subculture-modulated chondrocytes in agarose culture.

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