Studies of Schwann cell proliferation. II. Characterization of the stimulation and specificity of the response to a neurite membrane fraction.

Salzer, James L.; Williams, A. C.; Glaser, Luis; Bunge, R P

doi:10.1083/jcb.84.3.753

Cited by 259 publications

(121 citation statements)

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“…The mitogenic effect resulting from synergy between PITF, CT and FCS [5] is three times higher than that observed with neurite membrane fraction from sensory neurons [33,34]. The combined use of PITF and CT, has resulted in the accumulation of millions of cells with CT phenotype.…”

Section: Discussionmentioning

confidence: 99%

“…It has been suggested that SC indefinitely preserve their potential of migration even when they are fixed in the adult nerve. Migration resumes if nerve degeneration occurs [32].The mitogenic effect resulting from synergy between PITF, CT and FCS [5] is three times higher than that observed with neurite membrane fraction from sensory neurons [33,34]. The combined use of PITF and CT, has resulted in the accumulation of millions of cells with CT phenotype.…”

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confidence: 99%

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Structure and behavior of rat primary and secondary Schwann cells in vitro

Dubois‐Dalcq

Rentier

et al. 1981

Experimental Cell Research

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SUMMARYThe structure and motility of isolated rat primary (I) Schwann cells (SC) have been compared to that of subcultured (II) SC during and after mitotic stimulation. I SC contain myelin components which persist for 2 weeks in serum-free medium while they rapidly disappear in medium containing serum and high glucose concentration. These components were never detected in II SC. Both I SC and II SC after their mitotic phase are spindle-shaped, contain many intermediate and actin filaments, have no basement membrane but show intense migratory and undulatory activities. Rare fibroblasts in I cultures are recognized by their extremely variable shape, the presence of Thy 1.1 antigen in their membrane and their intense edge ruffling alternating with abrupt translocation. In contrast, I SC movements consist of intracellular translocation of nuclei along SC processes, which retract and extend constantly, and in slow rhythmic undulation episodes (2.3±0.2/min) alternating with migration at 135±50 µ/h. The total number of these episodes per day in serum-free medium is rigorously identical for different cells (166.3±0.2) and this uniformity of frequency suggests a genotypic basis. Cycles, consisting of an undulation episode followed by a resting interval, have mean durations of 8.6±4.1 min and a sharp peak of occurrence at 6 min, with exponential distribution of the longer periods. Motility of II SC is considerably inhibited during mitotic stimulation by cholera toxin and a pituitary extract while SC phenotype has changed to a flat multipolar cell with prominent Golgi and ribosomes. Migration is reduced to 24±2 µ/h and only 2 % of the SC show pulsations of the same periodicity as the I SC undulations. A dramatic increase in pulsation frequency occurs 6-12 h after removal of mitogenic factors when 80% of II SC start pulsating twice as fast for 2-3 days. When mitoses cease, SC quickly recover their SC phenotype with rhythmic undulations while migration speed increased to 92±20 µ/h. Thus, in spite of dramatic modification of shape, structure and behavior during mitotic stimulation, SC subsequently recover their unique motility pattern which might be essential for their myelinating function.Rat Schwann cells (SC), the myelin-form-ing cells of the peripheral nervous system, can now be cultured in isolation by using two different techniques [1][2][3]. In the first, rat dorsal root ganglia obtained just before birth are explanted and treated with antimitotic agents for a few days. After 10 days, the ganglia are excised and a "Schwann cell bed" is developed after the neurites are eliminated [1,2]. In the second technique, dissociation of newborn rat sciatic nerve results in a mixed population of SC and fibroblasts, which after 2 days of culturing are identified by their respective surface antigenic markers Ran 1 and Thy 1.1 [3,4]. In these cultures, fibroblast growth is first inhibited by AraC treatment and subsequently, by complement-mediated killing of Thy 1.1 positive cells [3]. SC growth can then be intensely stimulated by pi...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Structure and behavior of rat primary and secondary Schwann cells in vitro

Dubois‐Dalcq

Rentier

et al. 1981

Experimental Cell Research

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“…Neuregulins are produced by neurons (Marchionni et al, 1993;Dong et al, 1995) in a variety of splice variant transcripts, some of which encode a membrane-bound ligand (Marchionni et al, 1993). Immunohistochemical studies demonstrate neuregulins within axons , and neuronal membrane preparations stimulate the growth of cultured Schwann cells (Salzer et al, 1980) through the activation of p185 erbB2 (Morrissey et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Activation of ErbB2 during Wallerian Degeneration of Sciatic Nerve

et al. 1997

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We used anti-phosphopeptide-immunodetecting antibodies as immunohistochemical reagents to define the location and activity state of p185 erbB2 during Wallerian degeneration. Nerve damage induces a phosphorylation event at Y1248, a site that couples p185 erbB2 to the Ras-Raf-MAP kinase signal transduction pathway. Phosphorylation of p185 erbB2 occurs within Schwann cells and coincides in time and space with Schwann cell mitotic activity, as measured by bromodeoxyuridine uptake. These visual images of receptor autophosphorylation link activation of p185 erbB2 to the Schwann cell proliferation that accompanies nerve regeneration. Key words: neuregulin; erbB2; receptor tyrosine kinase; Schwann cell; Wallerian degeneration; phosphotyrosineUnlike elements of the C NS, peripheral nerves can regenerate when damaged. Understanding the regulation of this process has practical implications for treatment of peripheral neuropathies such as those secondary to diabetes, cancer chemotherapeutic agents, and other toxins. Moreover, insights into peripheral nerve regeneration may be transferable to treatment of spinal cord injuries. After peripheral nerves are damaged, they initially undergo Wallerian degeneration. Axons distal to the site of injury degenerate, and their myelin sheaths break down. Schwann cells then proliferate, providing a context for axonal regrowth and nerve regeneration (Waller, 1851;Fawcett and Keynes, 1990). Although Schwann cell proliferation is a prominent feature of nerve regeneration, the molecular signals driving the mitotic response have not been characterized.One viable candidate for regulating the Schwann cell proliferation that accompanies regeneration of peripheral nerves is the transmembrane tyrosine protein kinase p185 erbB2 . Schwann cells express p185 erbB2 both in culture and in vivo (Jin et al., 1993;Marchionni et al., 1993). The tyrosine kinase activity of p185 erbB2 is activated by a family of ligands known collectively as the neuregulins (glial growth factor, acetylcholine receptor-inducing activity, Neu differentiation factor, and heregulin) that are encoded as splice variant transcripts of a common gene. Neuregulins are expressed by neurons in the peripheral nervous system (Marchionni et al., 1993;Dong et al., 1995), and they promote the proliferation of Schwann cells in vitro (Marchionni et al., 1993;Marchionni, 1995;Morrissey et al., 1995).Activation of the p185 erbB2 tyrosine kinase results in the autophosphorylation of specific tyrosines on the intracellular domain of the receptor. This autophosphorylation can be monitored with anti-phosphotyrosine antibodies. However, reactivity with generic antibodies to phosphotyrosine provides no specific insight into the catalytic or signaling activities of a growth factor receptor. Moreover, anti-phosphotyrosine antibodies cannot be used as receptor-specific histochemical reagents. To determine the cellular location and activity state of p185 erbB2 during Wallerian degeneration, we exploited the fact that synthetic tyrosine phosphopeptides, cor...

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“…Membrane Purification-Sensory neuron membranes were isolated from DRG neurons, initially plated as explants but treated with cytosine arabinoside to remove all non-neuronal cells as described before (13,18) with modifications. The neurons were rinsed in PBS, and cell bodies were excised using a scalpel under a dissecting microscope.…”

Section: Methodsmentioning

confidence: 99%

Axonal Neuregulin 1 Type III Activates NF-κB in Schwann Cells during Myelin Formation

Limpert

Carter

2010

Journal of Biological Chemistry

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The formation of myelin requires a series of complex signaling events initiated by the axon to surrounding glial cells, which ultimately respond by tightly wrapping the axon with layers of specialized plasma membrane thereby allowing for saltatory conduction. Activation of the transcription factor NF-B in Schwann cells has been suggested to be critical for these cells to differentiate into a myelinating phenotype; however, the mechanisms by which it is activated have yet to be elucidated. Here, we demonstrate that axonal membranes are sufficient to pro-

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Studies of Schwann cell proliferation. II. Characterization of the stimulation and specificity of the response to a neurite membrane fraction.

Cited by 259 publications

References 22 publications

Structure and behavior of rat primary and secondary Schwann cells in vitro

Structure and behavior of rat primary and secondary Schwann cells in vitro

Activation of ErbB2 during Wallerian Degeneration of Sciatic Nerve

Axonal Neuregulin 1 Type III Activates NF-κB in Schwann Cells during Myelin Formation

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