S‐100 protein immunostaining identifies cells expressing a chondrocytic phenotype during articular cartilage repair

Abstract

The healing of articular surface defects has been studied with conventional histology, which relies on the staining of the extracellular matrix to identify the phenotype of the cells present. A chondrospecific cellular marker would be useful. S-100 protein has been found in all chondroid tissues studied, and we evaluated its usefulness in the study of articular cartilage repair. Full-thickness rabbit femoral condylar defects were made, and the specimens were studied at serial time intervals. S-100 protein staining positively showed chondroid cells in the 7- and 14-day specimens, which were not identifiable by conventional techniques. At 30 and 60 days, an S-100 positive band of cells separated a deep safranin-O positive hypertrophic layer from a fibrocellular surface layer. At 120 days, the presence of S-100 protein identified cells with chondrogenic potential, and the lack of S-100 protein in other cells embedded in conventionally stained matrix suggested that these cells were no longer of a chondroid phenotype. The presence of S-100 protein-identified chondroid cells early in the repair process when the cells had not begun to synthesize conventionally stainable matrix and the lack of S-100 protein in cells late in the repair positively identified a phenotypic change earlier than conventional histology.

Effects of hyaluronic acid and basic fibroblast growth factor on motility of chondrocytes and synovial cells in culture

“…They were cleared of adherent connective tissue and cut into small pieces. Chondrocytes were then isolated by enzymatic digestion (Wolff et al 1992). Brie y, cartilage specimens were minced and washed 3 times in sterile saline before isolating the chondrocytes rst with 0.25% trypsin in sterile saline for 30 min followed by 0.25% collagenase in DMEM supplemented with 10% heat-inactivated FBS and 1% penicillin (100 IU/mL)/streptomycin (100 m g/mL)/ amphotericin B (0.25 m g/mL) for 4-8 hrs at 37 °C in a culture bottle.…”

Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis

“…Activation of ERK MAP kinase and NF-B and increase in MMP-13 production in cultured chondrocytes by RAGE signaling. In order to provide further evidence that chondrocytes express functional RAGE, cells were first treated with S100B, which is a known RAGE ligand (7,8) and which has previously been described in chondrocytes (9). Treatment with S100B resulted in phosphorylation of the ERK-1/2 MAP kinase and the p65 subunit of NF-B ( Figure 5), both of which are well-characterized mediators of RAGE signaling (12,13).…”

“…RAGE is a member of the immunoglobulin superfamily and has been shown to be expressed by diverse cell types, including macrophages, endothelial cells, smooth muscle cells, myocytes, and neuronal cells (5,6). RAGE signaling has also been found to be stimulated by members of the S100 family of proteins, including S100B (7,8), which has been shown to be present in articular cartilage (9). An additional RAGE ligand is high mobility group box chromosomal protein 1 (HMGB-1; amphoterin) (10), which has recently been found to be expressed in OA cartilage (11).…”

Human articular chondrocytes on macroporous gelatin microcarriers form structurally stable constructs with blood-derived biological gluesin vitro

“…The chondrocytes did conversely stain positive for SOX-9 and S-100, two markers used for chondrocytic phenotype. S-100 is a calcium-binding protein that has been suggested and used as an identifying marker for the chondrocytic phenotype during articular cartilage repair previously [Wolff et al, 1992, Zheng et al, 2007. SOX-9 is a transcription factor that has been highly associated with the chondrocytic differentiation/chondrogenesis [Wehrli et al, 2003].…”