Changes in glycosaminoglycans during regeneration of post-crush sciatic nerves of adult guinea pigs

Upregulation of chondroitin 6-sulphotransferase-1 facilitates Schwann cell migration during axonal growth

“…Although increased chondroitin sulphates have been reported in injured peripheral nerves (Shum and Chau, 1996;Zuo et al, 1998), the fact that these are mainly soluble and extracellular has left the cellular source of the various sulphated chondroitin isoforms unclear. Attempts to target the core proteins of CSPGs found immunopositivities associated with non-neuronal elements of peripheral nerves -Schwann cells, perineurial and endoneurial fibroblasts, and blood vessels (Braunewell et al, 1995;Martin et al, 2001;Schneider et al, 2001;Rezajooi et al, 2004), but these at best indicated where the secreted or shed CSPGs were deposited.…”

“…Tuning of the pericellular environment is required to achieve optimum adhesiveness for the mobile phenotype. The increased chondroitin sulphate proteoglycans (CSPGs) reported in injured neural environments of adult mammals (Braunewell et al, 1995;Shum and Chau, 1996;Sandvig et al, 2004;Silver and Miller, 2004) suggest contribution to this effect. This is reinforced by in vitro studies which demonstrated expression of pericellular CSPGs as a requirement for invasive migration into a fibrin matrix (Henke et al, 1996;Clarke et al, 2004).…”

“…Nerve crush was performed on sciatic nerves of pentobarbital-anaesthetised (40 mg/kg body weight) male Sprague Dawley rats (200-250 g) as described (Shum and Chau, 1996). After 1, 3, 7, 14 and 28 days of recovery, animals were sacrificed by decapitation and the sciatic nerves were collected.…”

The DSD-1 Carbohydrate Epitope Depends on Sulfation, Correlates with Chondroitin Sulfate D Motifs, and Is Sufficient to Promote Neurite Outgrowth

“…In contrast to those findings, other studies have described either no or a stimulatory influence of chondroitin sulfate on neurite outgrowth (18,22,37,38). These results are in agreement with the findings that chondroitin sulfates are up-regulated after lesion during the period of sciatic nerve regeneration (39,40) and required for the regeneration of retinal goldfish axons (41). The divergence of results might have been caused by differences of the presentation of chondroitin sulfate and/or chondroitin sulfate PGs and by the use of distinct neuronal cell types.…”

“…This assumption is based on structural analysis, for example of CS-D (38,42,43), and on the immunohistological analysis of mAbs generated against chondroitin sulfates (44,45,71,72). These different mAbs yielded distinct spatial and temporal staining profiles in developing and in lesioned neural tissues (39,40,46). One further example is provided by the neurite outgrowth-promoting DSD-1 epitope, which is expressed in regions of intense axon growth in vivo, e.g.…”