## Abstract Fibronectin, a ubiquitous glycoprotein of the extracellular matrix, serves as a substrate for cell attachment. Binding to fibronectin through cell‐surface receptors promotes a flattened cell shape, stimulates the phosphorylation of intracellular protein, and changes the pattern of gene
Effects of growth-factor-enhanced culture on a chondrocyte-collagen implant for cartilage repair
✍ Scribed by Toolan, Brian C. ;Frenkel, Sally R. ;Pachence, James M. ;Yalowitz, Laurie ;Alexander, Harold
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 972 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0021-9304
No coin nor oath required. For personal study only.
✦ Synopsis
The effects of incubation and addition of growth factors to a chondrocyte-seeded collagen implant for cartilage repair were studied. Type I collagen matrices seeded with lapine articular chondrocytes and unseeded controls cultured in the presence and absence of fibroblast growth factor and insulin for 2, 6, and 9 weeks were subjected to biomechanical, biochemical, and histological analysis. Aggregate modulus of elasticity of seeded implants decreased by half at 6 weeks, then rose by a factor of 10 above initial values. Permeability of seeded implants and their controls decreased steadily. Glycosaminoglycan content peaked at 6 weeks, coinciding with the greatest number of chondrocytes and mitotic ac-tivity in seeded implants. Chondrocytes remained phenotypically stable and metabolically active; they incorporated glycosaminoglycan into the extracellular matrix, and formed an organized pericellular environment despite the predicted resorption of the collagen matrix. Adding fibroblast growth factor and insulin tripled the rate of cell turnover and doubled the glycosaminoglycan content of seeded implants, but had no effect on their material properties. In uitro incubation for 6 weeks in the presence of fibroblast growth factor and insulin creates a metabolically and mitotically active chondroc te collagen composite for implantation into articular cartiLge defects.
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