Leukocyte accumulation has been shown to be increased in sepsis. Moreover, in inducible nitric oxide synthase (iNOS) knockout mice, a further increase in leukocyte accumulation has been observed during sepsis, suggesting that nitric oxide (NO) may affect leukocyte/endothelial interaction. Accelerate
Effects of nitric oxide on chondrocyte migration, adhesion, and cytoskeletal assembly
β Scribed by Sally R. Frenkel; Robert M. Clancy; John L. Ricci; Paul E. di Cesare; John J. Rediske; Steven B. Abramson
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 885 KB
- Volume
- 39
- Category
- Article
- ISSN
- 0004-3591
No coin nor oath required. For personal study only.
β¦ Synopsis
Objective. The migration of cells of chondrocyte lineage is believed to play a role in cartilage growth and repair. The present study examined 1) whether chondrocytes are capable of migration in vitro; and 2) the effects of nitric oxide (NO) on chondrocyte migration, adhesion, and cytoskeletal assembly.
Methods. Chondrocyte migration was evaluated by 2 assays: 1) "centrifugal" migration within a 3dimensional collagen matrix (dot culture); and 2) directed migration under agarose in response to bone morphogenetic protein. To assess the effects of NO, chondrocytes were treated with either exogenous NO (S-nitrosoglutathione [SNO-GSH]) or a mixture of cytokines known to induce endogenous NO production. The effects of NO on chondrocyte adhesion to fibronectin-coated surfaces, as well as on actin polymerization (determined by indirect immunofluorescence), were also examined.
Results. The capacity of chondrocytes to migrate was demonstrated both by the dot culture and by agarose methods. Both SNO-GSH and endogenous NO induced by cytokines inhibited this migration. Exposure to NO also inhibited attachment of chondrocytes to fibronectin and disrupted assembly of actin filaments. These effects of SNO-GSH and cytokine-induced NO production were reversed in the presence of hemoglobin and the NO synthase inhibitor NG-monomethyl arginine, respectively.
Conclusion. NO interferes with chondrocyte mi-
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## Abstract **Summary:** Cell adhesion to a scaffold is a prerequisite for tissue engineering. Many studies have been focused on enhancing cell adhesion to synthetic materials that are used for scaffold fabrication. In this study, we applied an avidinβbiotin binding system to enhance chondrocyte ad