scholarly journals SCHWANN CELL PROLIFERATION IN DEVELOPING MOUSE SCIATIC NERVE

1967 ◽  
Vol 34 (3) ◽  
pp. 735-743 ◽  
Author(s):  
A. K. Asbury

Proliferation of Schwann cells in neonatal mouse sciatic nerve was studied radioautographically in 1-µ glycol methacrylate sections. 28 mice were injected with thymidine-3H, 4 µc/g, 48 hr after birth, and were killed serially over the next 4 days. For the cell cycle following injection, the generation time was approximately 24 hr as determined by grain-count halving data; the duration of synthesis phase was 8 hr as determined from a curve constructed from the per cent of mitotic figures containing label; and the labeling index was 9% at 2 hr after injection. With these estimates, the per cent of Schwann cells proliferating was calculated to be 27%. In addition, roughly 25% of dividing cells appeared to cease division during the cell cycle under study. The relationship of these findings to other events during maturation of nerve is discussed.

2013 ◽  
Vol 211 (1) ◽  
pp. 29-43 ◽  
Author(s):  
Emanuela Porrello ◽  
Cristina Rivellini ◽  
Giorgia Dina ◽  
Daniela Triolo ◽  
Ubaldo Del Carro ◽  
...  

Axonal sorting is a crucial event in nerve formation and requires proper Schwann cell proliferation, differentiation, and contact with axons. Any defect in axonal sorting results in dysmyelinating peripheral neuropathies. Evidence from mouse models shows that axonal sorting is regulated by laminin211– and, possibly, neuregulin 1 (Nrg1)–derived signals. However, how these signals are integrated in Schwann cells is largely unknown. We now report that the nuclear Jun activation domain–binding protein 1 (Jab1) may transduce laminin211 signals to regulate Schwann cell number and differentiation during axonal sorting. Mice with inactivation of Jab1 in Schwann cells develop a dysmyelinating neuropathy with axonal sorting defects. Loss of Jab1 increases p27 levels in Schwann cells, which causes defective cell cycle progression and aberrant differentiation. Genetic down-regulation of p27 levels in Jab1-null mice restores Schwann cell number, differentiation, and axonal sorting and rescues the dysmyelinating neuropathy. Thus, Jab1 constitutes a regulatory molecule that integrates laminin211 signals in Schwann cells to govern cell cycle, cell number, and differentiation. Finally, Jab1 may constitute a key molecule in the pathogenesis of dysmyelinating neuropathies.


2007 ◽  
Vol 3 (4) ◽  
pp. 269-279 ◽  
Author(s):  
Simona Loreti ◽  
Ruggero Ricordy ◽  
M. Egle De Stefano ◽  
Gabriella Augusti-Tocco ◽  
Ada Maria Tata

AbstractCultures of Schwann cells from neonatal rat sciatic nerves were treated with acetylcholine agonists and the effects on cell proliferation evaluated. 3[H]-thymidine incorporation shows that acetylcholine (ACh) receptor agonists inhibit cell proliferation, and FACS analysis demonstrates cell-cycle arrest and accumulation of cells in the G1 phase. The use of arecaidine, a selective agonist of muscarinic M2 receptors reveals that this effect depends mainly on M2 receptor activation. The arecaidine dependent-block in G1 is reversible because removal of arecaidine from the culture medium induces progression to the S phase. The block of the G1-S transition is also characterized by modulation of the expression of several cell-cycle markers. Moreover, treatment with ACh receptor agonist causes both a decrease in the PCNA protein levels in Schwann cell nuclei and an increase in p27 and p53 proteins. Finally, immuno-electron microscopy demonstrates that M2 receptors are expressed by Schwann cells in vivo. These results indicate that ACh, by modulating Schwann cell proliferation through M2 receptor activation, might contribute to their progression to a more differentiated phenotype.


1980 ◽  
Vol 84 (3) ◽  
pp. 739-752 ◽  
Author(s):  
J L Salzer ◽  
R P Bunge

In this paper the stimuli for and pattern of Schwann cell proliferation are defined under various experimental conditions. We used a tissue culture system in which fetal rat dorsal root ganglia, treated to eliminate contaminating fibroblasts (Wood, P., 1976, Brain Res. 115:361--375), appear to recapitulate many aspects of the developing peripheral nervous system. We observed that: (a) proliferation of Schwann cells on neurites is initially rapid, but, as each neurite becomes fully ensheathed, division slows considerably and is confined to the periphery of the outgrowth; (b) during the period of rapid proliferation, excision of the ganglion causes a rapid decay in the number of dividing cells; (c) excision of the ganglion from more established cultures in which there was little ongoing proliferation resulted in a small increase in labeling at the site of excision for all Schwann cells and a substantial increase in labeling for myelin-related cells with a peak labeling period at 4 d; (d) direct mechanical injury during Wallerian degeneration is mitogenic for Schwann cells; (e) a variety of potential mitogens failed to stimulate Schwann cell proliferation, and (f) replated cells have a slightly higher level of proliferation and show a small and variable response to the addition of cAMP.


1973 ◽  
Vol 13 (2) ◽  
pp. 461-477
Author(s):  
SUSAN M. HALL

The morphology of remyelination following demyelination induced by the intraneural injection of lysophosphatidyl choline, LPC, has been examined in the mouse sciatic nerve, at periods up to 240 days post-injection. It was found that, in many fibres, the process resembled primary myelinogenesis. There was a moderate Schwann cell proliferation; those Schwann cells not involved in remyelination remained closely associated with the remyelinating Schwann cell/axon unit, within a common basal lamina tube. Numerous small axons, considered to be sprouts from the remyelinating axon, were observed lying in contact with the ‘supernumerary Schwann cells’. In a small population of fibres, however, atypical morphological features were consistently seen: (i) multiple mesaxons, indicating probable remyelination by tunication; (ii) paranodal reorganization in the junctional zone; (iii) the formation of internodal ‘pseudonodes’, which subsequently underwent transition into incisures of Schmidt-Lanterman. These structures are discussed in terms of the re-establishment of the Schwann cell/axon relationship.


2015 ◽  
Vol 56 (1) ◽  
pp. 216-227 ◽  
Author(s):  
Youhua Wang ◽  
Shiran Zhou ◽  
Hua Xu ◽  
Shixian Yan ◽  
Dawei Xu ◽  
...  

Blood ◽  
1970 ◽  
Vol 35 (6) ◽  
pp. 761-774 ◽  
Author(s):  
BERNARD S. MORSE ◽  
NICHOLAS J. RENCRICCA ◽  
FREDERICK STOHLMAN

Abstract Hydroxyurea, a cytotoxic agent that kills cells in DNA synthesis, was used to study the relationship between erythropoietin and the generative cycle of the immediate erythroid precursor cell. When OHU and EP were administered simultaneously to hypertransfused mice, the resultant erythroid response was diminished relative to EP treated controls. OHU given at intervals after EP resulted in a progressively greater diminution of erythroid response. From these studies, then, we would suggest that in the suppressed animal the committed stem cell compartment is in cycle but with a prolonged G1. After EP there is a shortening of the generation time and an increase in the rate of turnover of the committed stem cells. The data also indicate that cells in cycle are differentiated into the pronormoblast compartment. It further may be suggested that erythropoietin is effective throughout the bulk of the generative cycle although it seems unlikely that differentiation is accomplished during the mitotic phase. Whether erythropoietin must be present in both G1 and S as suggested by Kretchmar cannot be answered by the present studies. The data also indicate that cells of the pluripotential compartment are normally in G0 or perhaps a prolonged G1. Damage to the committed compartment appears to be in part repaired by the influx of cells from the pluripotential compartment.


Blood ◽  
1966 ◽  
Vol 28 (3) ◽  
pp. 428-445 ◽  
Author(s):  
ALVIN M. MAUER ◽  
VIRGINIA FISHER

Abstract The characteristics of proliferation of leukemic cells in four children with untreated acute leukemia have been studied. In all four of these children a population of marrow leukemic cells was found which were dividing with a generation time of about 15 to 20 hours. In two of these patients it was possible to demonstrate that these dividing cells after one or more mitotic divisions became smaller and stopped dividing. In all of these patients 70 per cent or more of the leukemic cells of the marrow and almost all leukemic cells of the blood were nonproliferative at the time of these studies. These nondividing cells would be relatively unaffected by chemotherapeutic agents designed to inhibit cell division.


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