Identification of the major proteins that promote neuronal process outgrowth on Schwann cells in vitro.

Bixby, John L.; Lilien, Jack; Reichardt, Louis F.

doi:10.1083/jcb.107.1.353

Cited by 402 publications

(242 citation statements)

References 76 publications

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“…Antibodies against N-cadherin inhibit neurite outgrowth in vitro on astrocytes and Schwann cells (Tomaselli et al, 1988;Bixby et al, 1988). In general, antibodies against cadherins disrupt cell-cell contacts.…”

Section: Discussionmentioning

confidence: 99%

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Expression of cell adhesion molecules during initiation and cessation of neural crest cell migration

Akitaya

Bronner‐Fraser

1992

Developmental Dynamics

173

115

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Because of their distribution and known ability to promote neuronal adhesion, it has been proposed that N-CAM and N-cadherin are involved in the formation of the nervous system. Here, we examine the expression of these molecules during the initiation and cessation of trunk neural crest cell migration during the formation of the peripheral nervous system. Whereas other neural tube cells express N-cadherin, the dorsal neural tube containing neural crest precursors has little or no N-cadherin immunoreactivity. In contrast, N-CAM is expressed in the dorsal neural tube and on early migrating neural crest cells, from which it gradually disappears during migration. Both N-CAM and N-cadherin are absent from neural crest cells at advanced stages of migration. As neural crest cells cease migration and condense to form dorsal root and sympathetic ganglia, N-cadherin but not N-CAM is observed on the forming ganglia, identified by neurofilament expression and the aggregation of HNK-1 reactive cells. The results demonstrate that the absence of N-cadherin correlates with the onset of neural crest migration and its reappearance correlates with cessation of migration and precedes gangliogenesis. 0 1992 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

“…Injection of N-cadherin mRNA into early frog embryos results in abnormal nervous system formation (Detrick et al, 1990). Antibodies against N-cadherin inhibit neurite outgrowth in vitro on astrocytes and Schwann cells (Tomaselli et al, 1988;Bixby et al, 1988) and disrupt 0 1992 WILEY-LISS, INC somite explants into single cell sheets .…”

Section: Introductionmentioning

confidence: 99%

Expression of cell adhesion molecules during initiation and cessation of neural crest cell migration

Akitaya

Bronner‐Fraser

1992

Developmental Dynamics

173

115

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“…All of these factors are prerequisites for the survival and axonal regeneration of damaged neurons. [7][8][9] Neurotropin-3 (NT-3) is one of the important neurotrophic factors. It can prevent atrophy of mature CNS neurons, and promote corticospinal tract axonal regeneration and recovery of hindlimb's function in spinal cord injured animal [10][11][12][13][14][15] and Hapner et al 16 had indicated that NT-3 could upregulate the TrkC expression of NSCs and promote for them to differentiate into neurons.…”

Section: Introductionmentioning

confidence: 99%

Cotransplant of neural stem cells and NT-3 gene modified Schwann cells promote the recovery of transected spinal cord injury

Guo

Zeng

et al. 2006

Spinal Cord

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Study design: An animal model of transected spinal cord injury (SCI) was used to test the hypothesis that cografted neural stem cells (NSCs) and NT-3-SCs promote morphologic and functional recoveries of injured spinal cord. Objective: To explore whether cotransplant of NSCs and NT-3-SCs could promote the injured spinal cord repair. Setting: Zhongshan Medical College, Sun Yat-sen University, PR China. Methods: Female Sprague-Dawley (SD) rats weighing on 200-220 g were used to prepare SCI models. The spinal cord was transected between T 9 and T 10 , then NSCs, SCs þ NSCs, LacZSCs þ NSCs, or NT-3-SCs þ NSCs were grafted into the transected site. Results: (1) Part of NSCs could differentiate to neuron-like cells in the transected site and the percentage of differentiation was NT-3-SCs þ NSCs group4SCs þ NSCs group4NSCs group. (2) In the grafted groups, there were 5-HT, CGRP, and SP positive nerve fibres within the transected site. Some fluorogold (FG)-labeled cells were found in the spinal cord rostral to the transected site, the red nuclei and the inner pyramidal layer of sensorimotor cortex. (3) The cells grafted could enhance the injured neurons survival in inner pyramidal layer of sensorimotor cortex, red nuclei of midbrain, and Clark's nuclei of spinal cord's L1 segment, could decrease the latency and increase the amplitude of cortical somatosensory evoked potential (CSEP) and cortical motor evoked potential (CMEP), and could promote partly structural and functional recovery of the SCI rats.Conclusion: These results demonstrate that cografted NT-3-SCs and NSCs is a potential therapy for SCI.

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“…First, antibodies recognizing N-cadherin inhibit neurite growth on the surfaces of several types of nonneuronal cells (e.g., Bixby et al, 1987Bixby et al, , 1988Tomaselli et al, 1988). Second, immortal cells transfected with a cDNA clone of the gene encoding N-cadherin are a much better substrate for neurite growth from retinal explants than the control, untransfected cells (Matsunaga et al, 1988a).…”

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confidence: 99%

“…More recently, examination of process outgrowth induced by the surfaces of other cells has strongly suggested a role for cell adhesion molecules in this process (Bixby et al, 198% 1988;Chang et al, 1987;Tomaselli et al, 1988;Seilheimer and Schachner, 1988). The particular cell adhesion molecules that are involved include L1 Lagenauer and Lemmon, 1987;Bixby et al, 1988); the Ll-related molecules, FI1 (contactin) and neurofascin Rathjen et al, 1987;Brummendorf et al, 1989;Ranscht, 1988); neural cell adhesion molecule (N-CAM) (Bixby et al, 1987;Neugebauer et al, 1988;Doherty et al, 1989); and N-cadherin (references cited above). Some evidence suggests that the myelin-associated glycoprotein may also be involved in neurite extension (Johnson et al, 1989).…”

mentioning

confidence: 99%

Purified N-cadherin is a potent substrate for the rapid induction of neurite outgrowth.

Bixby

Zhang

1990

The Journal of Cell Biology

Self Cite

267

171

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Abstract. N-cadherin is the predominant mediator of calcium-dependent adhesion in the nervous system (Takeichi, M. 1988. Development (Camb. Takeichi. 1988. Nature (Lond.). 334:62-64) have provided evidence that N-cadherin, alone or in combination with other molecules, can participate in the induction of neurite extension. We have developed an affinity purification procedure for the isolation of whole N-cadherin from chick brain and have used the isolated protein as a substrate for neurite outgrowth. N-cadherin promotes the rapid extension of neurites from chick ciliary ganglion neurons, which extend few or no neurites on adhesive but noninducing substrates such as polylysine, tissue culture plastic, and collagens. N-cadherin is extremely potent, more so than the L1 adhesion molecule, and comparable to the extracellular matrix protein laminin. Compared to laminin, however, N-cadherin promotes outgrowth from ciliary ganglion neurons extremely rapidly and with a distinct morphology. These results provide a direct demonstration that N-cadherin is sufficient to induce neurite outgrowth when substrate bound and suggest that the mechanism(s) involved may differ from that induced by laminin.

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Identification of the major proteins that promote neuronal process outgrowth on Schwann cells in vitro.

Cited by 402 publications

References 76 publications

Expression of cell adhesion molecules during initiation and cessation of neural crest cell migration

Expression of cell adhesion molecules during initiation and cessation of neural crest cell migration

Cotransplant of neural stem cells and NT-3 gene modified Schwann cells promote the recovery of transected spinal cord injury

Purified N-cadherin is a potent substrate for the rapid induction of neurite outgrowth.

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