Schwannoma cell-derived inhibitor of the neurite-promoting activity of laminin.

Muir, David; Engvall, Eva; Varon, S; Manthorpe, Marston

doi:10.1083/jcb.109.5.2353

Cited by 88 publications

(47 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…6,7 Because CSPG is able to directly bind to laminin, at least in vitro, [75][76][77][78] cleavage of CSPG in laminin-rich blood vessel BM might well affect the structure of these membranes and increase their detachment and separation. This effect of CSPG degradation appears to also concern blood vessel-independent laminin deposits, because we noted less streamer deposits in treated animals, associated with a slight decrease in laminin protein levels during the first weeks after SCI.…”

Section: Discussionmentioning

confidence: 99%

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Milbreta

Boxberg

Mailly

et al. 2014

Journal of Neurotrauma

View full text Add to dashboard Cite

Upregulation of extracellular chondroitin sulfate proteoglycans (CSPG) is a primary cause for the failure of axons to regenerate after spinal cord injury (SCI), and the beneficial effect of their degradation by chondroitinase ABC (ChABC) is widely documented. Little is known, however, about the effect of ChABC treatment on astrogliosis and revascularization, two important factors influencing axon regrowth. This was investigated in the present study. Immediately after a spinal cord hemisection at thoracic level 8-9, we injected ChABC intrathecally at the sacral level, repeated three times until 10 days post-injury. Our results show an effective cleavage of CSPG glycosaminoglycan chains and stimulation of axonal remodeling within the injury site, accompanied by an extended period of astrocyte remodeling (up to 4 weeks). Interestingly, ChABC treatment favored an orientation of astrocytic processes directed toward the injury, in close association with axons at the lesion entry zone, suggesting a correlation between axon and astrocyte remodeling. Further, during the first weeks post-injury, ChABC treatment affected the morphology of laminin-positive blood vessel basement membranes and vessel-independent laminin deposits: hypertrophied blood vessels with detached or duplicated basement membrane were more numerous than in lesioned untreated animals. In contrast, at later time points, laminin expression increased and became more directly associated with newly formed blood vessels, the size of which tended to be closer to that found in intact tissue. Our data reinforce the idea that ChABC injection in combination with other synergistic treatments is a promising therapeutic strategy for SCI repair.

show abstract

Section: Discussionmentioning

confidence: 99%

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Milbreta

Boxberg

Mailly

et al. 2014

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

“…HSPG^laminin complexes also modulate neurite outgrowth in vitro including growth promotion and growth inhibition (Lander et al, 1985a,b;Chiu et al, 1986;Hantaz-Ambroise et al, 1987;Mathiessen et al, 1989). For example, whereas monoclonal antibodies to HSPG reduce neurite outgrowth on sciatic nerve in vitro (Sandrock and Matthew, 1985) a Schwannoma-derived HSPG also blocks the neurite-promoting activity of laminin (Muir et al, 1989). Interestingly, HSPGs do not appear necessary for neurite outgrowth on astrocytes (Ard and Bunge, 1988).…”

Section: Heparan Sulphate Proteoglycansmentioning

confidence: 99%

Relationship between sprouting axons, proteoglycans and glial cells following unilateral nigrostriatal axotomy in the adult rat

et al. 2002

View full text Add to dashboard Cite

AbstractöProteoglycans may modulate axon growth in the intact and injured adult mammalian CNS. Here we investigate the distribution and time course of deposition of a range of proteoglycans between 4 and 14 days following unilateral axotomy of the nigrostriatal tract in anaesthetised adult rats. Immunolabelling using a variety of antibodies was used to examine the response of heparan sulphate proteoglycans, chondroitin sulphate proteoglycans and keratan sulphate proteoglycans. We observed that many proteoglycans became abundant between 1 and 2 weeks post-axotomy. Heparan sulphate proteoglycans were predominantly found within the lesion core (populated by blood vessels, amoeboid macrophages and meningeal ¢broblasts) whereas chondroitin sulphate proteoglycans and keratan sulphate proteoglycans were predominantly found in the lesion surround (populated by reactive astrocytes, activated microglia and adult precursor cells). Immunolabelling indicated that cut dopaminergic nigral axons sprouted proli¢cally within the lesion core but rarely grew into the lesion surround.We conclude that sprouting of cut dopaminergic nigral axons may be supported by heparan sulphate proteoglycans but restricted by chondroitin sulphate proteoglycans and keratan sulphate proteoglycans. ß

show abstract

“…An important issue that this work does not address is whether LRE is exposed and active in the environments that neurons or neurites actually encounter in vivo. In fact, some adhesive sites demonstrable on fragments of laminin are now believed to be inaccessible or "latent" in the native molecule (Nurcombe et al, 1989), and others may be masked in the complexes that laminin forms with other matrix molecules (e.g., Muir et al, 1989).…”

Section: Lre-dependent Adhesion To Native Basal Laminaementioning

confidence: 99%

“…These results provide the first clue to the functional consequences of LRE-dependent adhesion. However, a variety of processes could result in an apparent inhibition of neurite outgrowth (Patterson, 1988;Muir et al, 1989;Keynes and Cook, 1990;Schwab, 1990) and further experiments will be required to distinguish among them. For example, activation of an LRE-dependent system could prevent the initiation of neurites, decrease their rate of elongation, or cause their retraction.…”

Section: Lre-dependent Adhesion Of Motoneuron-like Cellsmentioning

confidence: 99%

An LRE (leucine-arginine-glutamate)-dependent mechanism for adhesion of neurons to S-laminin

et al. 1991

View full text Add to dashboard Cite

S-laminin is a homolog of laminin that is concentrated in the synaptic cleft of the neuromuscular junction. We previously showed that the tripeptide LRE is a crucial determinant for binding of ciliary motoneurons to recombinant s-laminin. Here, we describe a neuroblastoma- spinal neuron hybrid cell line, NSC-34, that binds to an LRE-containing s-laminin fragment and to a synthetic LRE-protein conjugate. NSC-34 cells exhibit several properties of motoneurons; other cell lines tested were not motoneuron-like and did not display LRE-dependent adhesion. We therefore used NSC-34 cells to characterize the LRE- dependent adhesion mechanism. Inhibition studies with a series of 20 tripeptide LRE analogs showed that the cells exhibit a high degree of selectivity for LRE, and suggested that ligand binding requires a combination of electrostatic and hydrophobic interactions. The effects of cations on LRE-dependent adhesion are unlike those of previously described adhesion molecules including the integrins, a family of receptors for extracellular matrix proteins, including laminin. Specifically, adhesion to LRE does not require divalent cations and is inhibited by Ca2+ (but not by Mg2+) in the physiological range. In contrast, adhesion of NSC-34 cells to laminin is LRE- and Ca2+ independent but Mg2+ dependent, and appears to be mediated by integrins. Additionally, experiments using mixed substrates demonstrated that LRE-protein conjugates inhibit neurite outgrowth promoted by laminin. Finally, we show that, under ionic conditions that minimize integrin-dependent adhesion, NSC-34 cells bind to s-laminin- rich basal laminae in tissue sections in an LRE-dependent manner. Together, these results suggest that LRE comprises a motoneuron- selective adhesion site that is accessible in native basal laminae and that acts to inhibit neurite outgrowth.

show abstract

Schwannoma cell-derived inhibitor of the neurite-promoting activity of laminin.

Cited by 88 publications

References 37 publications

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment

Relationship between sprouting axons, proteoglycans and glial cells following unilateral nigrostriatal axotomy in the adult rat

An LRE (leucine-arginine-glutamate)-dependent mechanism for adhesion of neurons to S-laminin

Contact Info

Product

Resources

About