scholarly journals Inactivation of one allele of the type II collagen gene alters the collagen network in murine articular cartilage and makes cartilage softer

2001 ◽  
Vol 60 (3) ◽  
pp. 262-268 ◽  
Author(s):  
M M Hyttinen
Keyword(s):  
Articular Cartilage ◽  
Type Ii Collagen ◽  
Collagen Gene ◽  
Type Ii ◽  
Collagen Network

Detection of MMP-13 Activity on Intentionally Strain-Released Type-II Collagen Network in Bovine Articular Cartilage

2011 ◽  
Author(s):  
Nazli Caner ◽  
Jeffrey W. Ruberti
Keyword(s):  
Articular Cartilage ◽  
Degradation Kinetics ◽  
Type Ii Collagen ◽  
Healthy Tissue ◽  
Cartilage Explants ◽  
Cartilage Tissue ◽  
Mechanical Stimuli ◽  
Type Ii ◽  
Collagen Network ◽  
Mechanical Tension

Articular cartilage is a specialized avascular connective tissue found at the contact regions of diarthrodial joints. Cartilage has few cells (< 5% of the volume), though these cells can maintain the balance of turnover in healthy tissue, when the tissue is damaged, they are not able to repair the defects [1–3]. Extra cellular matrix (ECM) in cartilage comprises water, collagen (principally type II), proteoglycans and noncollagenous proteins. The type II collagen network, which is the dominant structural protein in cartilage ECM, constrains the expansion of the resident PGs and is generally held in mechanical tension. In osteoarthritis (OA), the balance of cartilage tissue production/degradation is thought to be affected by abnormal mechanical stimuli leading to net matrix resorption through production of excess degradative enzymes (e.g. matrix metalloproteinases (MMP) and aggrecanases) [4–8]. In OA tissue the amount of MMP-13 is thought to be increased relative to healthy tissue. OA typically occurs in older adults where, as cartilage ages, there is a marked decrease in the fixed charge density (FCD), the hydration and, consequently, mechanical tension on the collagen type II network [9–11]. We have hypothesized that loss of tension on the collagen network accelerates degradation by MMP. Detection of the effect of MMP on loaded, native cartilage could lead to insight about cartilage degradation kinetics in OA. However, it is quite difficult to controllably deliver MMP to cartilage, to activate the MMP during detensioning of the collagen network and to detect the effect on the cartilage mechanics (because cost limits the amount of MMP used). We have developed a transpirational enzyme loading method which is capable of precisely dosing bovine cartilage explants with a small, known quantity of MMP-13. Following enzyme insertion, we are able to detect the activity of the MMP on osmotically compressed cartilage (i.e. cartilage with a detensioned collagen network) via a simple hydration measurement.

scholarly journals Boosting the Intra-Articular Efficacy of Low Dose Corticosteroid through a Biopolymeric Matrix: An In Vivo Model of Osteoarthritis

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1571
Author(s):  
Matilde Tschon ◽  
Francesca Salamanna ◽  
Lucia Martini ◽  
Gianluca Giavaresi ◽  
Luca Lorenzini ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Pain Sensitivity ◽  
Type Ii Collagen ◽  
Male Rats ◽  
In Vivo Model ◽  
Type Ii ◽  
Chemical Induction ◽  
Local Pain ◽  
Gait Parameters

The purpose of this study was to verify the efficacy of a single intra-articular (i.a.) injection of a hyaluronic acid-chitlac (HY-CTL) enriched with two low dosages of triamcinolone acetonide (TA, 2.0 mg/mL and 4.5 mg/mL), in comparison with HY-CTL alone, with a clinical control (TA 40 mg/mL) and with saline solution (NaCl) in an in vivo osteoarthritis (OA) model. Seven days after chemical induction of OA, 80 Sprague Dawley male rats were grouped into five arms (n = 16) and received a single i.a. injection of: 40 mg/mL TA, HY-CTL alone, HY-CTL with 2.0 mg/mL TA (RV2), HY-CTL with 4.5 mg/mL TA (RV4.5) and 0.9% NaCl. Pain sensitivity and Catwalk were performed at baseline and at 7, 14 and 21 days after the i.a. treatments. The histopathology of the joint, meniscus and synovial reaction, type II collagen expression and aggrecan expression were assessed 21 days after treatments. RV4.5 improved the local pain sensitivity in comparison with TA and NaCl. RV4.5 and TA exerted similar beneficial effects in all gait parameters. Histopathological analyses, measured by Osteoarthritis Research Society International (OARSI) and Kumar scores and by immunohistochemistry, evidenced that RV4.5 and TA reduced OA features in the same manner and showed a stronger type II collagen and aggrecan expression; both treatments reduced synovitis, as measured by Krenn score and, at the meniscus level, RV4.5 improved degenerative signs as evaluated by Pauli score. TA or RV4.5 treatments limited the local articular cartilage deterioration in knee OA with an improvement of the physical structure of articular cartilage, gait parameters, the sensitivity to local pain and a reduction of the synovial inflammation.

Finite Element Modeling of Osmotic Swelling in Tissue-Engineered Cartilage

2008 ◽  
Author(s):  
Liming Bian ◽  
Terri Ann N. Kelly ◽  
Eric G. Lima ◽  
Gerard A. Ateshian ◽  
Clark T. Hung
Keyword(s):  
Articular Cartilage ◽  
Potential Role ◽  
Swelling Pressure ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Osmotic Swelling ◽  
Fixed Charges ◽  
Central Regions ◽  
Significant Research ◽  
Engineered Cartilage

Proteoglycans and Type II collagen represent the two major biochemical constituents of articular cartilage. Collagen fibrils in cartilage resist the swelling pressure that arises from the fixed charges of the glycosaminoglycans (GAGs), and together they give rise to the tissue’s unique load bearing properties. As articular cartilage exhibits a poor intrinsic healing capacity, there is significant research in the development of cell-based therapies for cartilage repair. In some of our tissue engineering studies, we have observed a phenomenon where chondrocyte-seeded hydrogel constructs display cracking in their central regions after significant GAG content has been elaborated in culture. A theoretical analysis was performed to gain greater insights into the potential role that the spatial distribution of proteoglycan and collagen may play in this observed response.

Down-regulation of chondrocyte aggrecan and type-II Collagen gene expression correlates with increases in static compression magnitude and duration

1999 ◽  
Vol 17 (6) ◽  
pp. 836-842 ◽  
Author(s):  
Paula M. Ragan ◽  
Alison M. Badger ◽  
Michael Cook ◽  
Vicki I. Chin ◽  
Maxine Gowen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type Ii Collagen ◽  
Collagen Gene ◽  
Type Ii ◽  
Down Regulation ◽  
Static Compression ◽  
Collagen Gene Expression

scholarly journals The Effects of Proteoglycan and Type II Collagen on T1ρ Relaxation Time of Articular Cartilage

2015 ◽  
Vol 72 (2) ◽  
pp. 108
Author(s):  
Won Seok Choi ◽  
Hye Jin Yoo ◽  
Sung Hwan Hong ◽  
Ja-Young Choi
Keyword(s):  
Relaxation Time ◽  
Articular Cartilage ◽  
Type Ii Collagen ◽  
Type Ii

scholarly journals Tissue-specific expression of the human type II collagen gene in mice.

1987 ◽  
Vol 84 (9) ◽  
pp. 2803-2807 ◽  
Author(s):  
R. H. Lovell-Badge ◽  
A. Bygrave ◽  
A. Bradley ◽  
E. Robertson ◽  
R. Tilly ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Collagen Gene ◽  
Type Ii ◽  
Specific Expression ◽  
Tissue Specific ◽  
Tissue Specific Expression ◽  
Human Type
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