The thickness of the articular cartilage was determined using an established technique in which a sharp needle was pushed through the cartilage layer and into the underlying bone, using a testing machine [ 3, 18].
Using an established juvenile bovine model system, engineered cartilage was preconditioned with low doses of IL-1α (0.1 ng/mL, 0.5 ng/mL, and 1.0 ng/mL) for 7 days before exposure to an insult dose (10 ng/mL).
Cartilage sections (5 μm thick) were stained with safranin O-fast green using an established protocol [ 50] to detect the glycosaminoglycan (GAG) positive matrix that is typical for the hyaline cartilage and normally stains red.
All histological and IHC sections were blindly evaluated using a previously established grading scale detailing the severity of OA characteristics in equine cartilage [ 25].
NHAC-kn were derived from a single-donor knee articular cartilage and used as an established normal chondrocyte cell line [ 27, 28].
The effects of HDAC inhibitors on cartilage degradation were assessed using a bovine nasal cartilage explant assay.
The aim of the present study was therefore to determine the changes in cartilage PRG4 expression and immunolocalisation occurring early in the pathogenesis of OA with the use of an established animal model.
This involved using an explant model of cartilage to investigate the secretome of canine articular cartilage.
In this study, we have examined the potential of tissue-engineered cartilage analogs developed using different cell types, i.e., mesenchymal stem cells (MSCs) vs chondrocytes and de-differentiated chondrocytes, in an established "construct in cartilage ring" model.
We have established two growth plate-derived chondrocyte cell lines, MMR14 and MMR17, from p53−/− mice (Nakamata T, Aoyama T, Okamoto T, Hosaka T, Nishijo K, Nakayama T, et al. In vitro demonstration of cell-to-cell interaction in growth plate cartilage using chondrocytes established from p53−/− mice. J Bone Miner Res 2003 18 97 107).
