scholarly journals Establishment of immortalized Schwann cells derived from rat embryo dorsal root ganglia

2012 ◽  
Vol 30 (3) ◽  
pp. 480-486 ◽  
Author(s):  
HUAJUN JIANG ◽  
WEI QU ◽  
FENG HAN ◽  
DAZHUANG LIU ◽  
WEIGUO ZHANG
BioTechniques ◽  
2019 ◽  
Vol 67 (1) ◽  
pp. 11-15
Author(s):  
Zhuowen Liang ◽  
Tao Lei ◽  
Shuang Wang ◽  
ZhuoJing Luo ◽  
XueYu Hu

2007 ◽  
Vol 208 (2) ◽  
pp. 285-296 ◽  
Author(s):  
Pei-Lin Zhang ◽  
Alon M. Levy ◽  
Levana Ben-Simchon ◽  
Shalom Haggiag ◽  
Judith Chebath ◽  
...  

Biomaterials ◽  
2012 ◽  
Vol 33 (33) ◽  
pp. 8529-8539 ◽  
Author(s):  
Rodolfo E. Gámez Sazo ◽  
Katsumi Maenaka ◽  
Weiyong Gu ◽  
Patrick M. Wood ◽  
Mary Bartlett Bunge

1973 ◽  
Vol 21 (1) ◽  
pp. 34-41 ◽  
Author(s):  
ELENA CITKOWITZ ◽  
ERIC HOLTZMAN

Bodies with the morphologic and cytochemical characteristics of peroxisomes have been identified in the satellite and Schwann cells of rat dorsal root ganglia. They are membrane-delimited, round or oval structures which contain a moderately electron-dense matrix but lack a crystalline core. On incubation of the tissue in a cytochemical medium for demonstration of peroxisomes, these bodies show heavy deposits of reaction product. The reaction is inhibited by heating the tissue or by incubation in the presence of aminotriazole or dichlorophenolindophenol. In tissue incubated for acid phosphatase activity the bodies are not reactive, although lysosomes show reaction product.


2021 ◽  
Vol 23 (Supplement_4) ◽  
pp. iv7-iv7
Author(s):  
Charlotte Lespade ◽  
Liyam Laraba ◽  
Evyn Woodhouse ◽  
Marie Srotyr ◽  
Alison C Lloyd ◽  
...  

Abstract Aims The NF2 gene encodes the tumour suppressor Merlin, which is deleted in 100% of patients with the familial tumour predisposition syndrome neurofibromatosis type 2 but also in 70% of those who develop sporadic schwannomas. The Raf-TR mouse model uses a tamoxifen-inducible Raf-kinase/ oestrogen receptor fusion protein (Raf-TR) expressed in myelinating Schwann cells to mimic a nerve injury response in Schwann cell by activating Raf/MEK/ERK signalling in the absence of peripheral nerve injury. We will assess whether Raf/MEK/ERK activation on an NF2 null background leads to tumourigenesis within the vestibular nerves and dorsal root ganglia (DRGs), two tumour sites identified in the Periostin-Cre mouse model in which schwannoma formation is spontaneous, with a view to generating an inducible NF2 null schwannoma mouse model. Method Mice with a Schwann cell specific loss of Merlin were crossed with mice carrying a tamoxifen-inducible Raf-TR gene to generate Raf-TR+/-; P0-Cre+/-; NF2fl/fl (Cre+) mice which were NF2 null and compared to Raf-TR+/-; P0-Cre-/-; NF2fl/fl (Cre-) littermate controls. Mice were injected with tamoxifen or vehicle for five consecutive days and their vestibular nerves and dorsal root ganglia (DRGs) were analysed at various timepoints . An EdU proliferation assay was used to quantify the proliferation in the vestibular ganglia, as well as the DRGs. Rates of proliferation were compared to Cre- age-matched littermate controls treated with tamoxifen or vehicle. Results In the Periostin-Cre NF2 null schwannoma model, tumours form spontaneously in the DRGs and vestibular ganglia. In our new model, we see a clear increase in proliferation at 21 d post-injection in the NF2 null (Cre+) tamoxifen-treated mice compared to control (Cre-) tamoxifen-treated controls in both DRGs and vestibular ganglia. Cre- tamoxifen-treated mice do not show increased proliferation compared to Cre- vehicle controls. Taken together, this shows that activation of the Raf/MEK/ERK pathway in Schwann cells only causes a sustained proliferation response on an NF2 null background in the DRGs and vestibular ganglia. We are assessing later timepoints to further characterise tumour development in these mice. Conclusion Combining the Raf-TR mouse model to create a demyelinating phenotype with an NF2 null background leads to vastly increased rates of proliferation at the sites of schwannoma tumourigenesis within the peripheral nervous system: the DRGs and the vestibular ganglia. The high proliferation in the vestibular ganglia in particular is similar to the development of vestibular schwannomas in patients with Neurofibromatosis type 2. The new mouse model used in this study shows potential to be very useful as an inducible schwannoma tumour model, in which we can study the early events of tumour formation.


Science ◽  
2014 ◽  
Vol 345 (6192) ◽  
pp. 87-90 ◽  
Author(s):  
I. Espinosa-Medina ◽  
E. Outin ◽  
C. A. Picard ◽  
Z. Chettouh ◽  
S. Dymecki ◽  
...  

Neural crest cells migrate extensively and give rise to most of the peripheral nervous system, including sympathetic, parasympathetic, enteric, and dorsal root ganglia. We studied how parasympathetic ganglia form close to visceral organs and what their precursors are. We find that many cranial nerve-associated crest cells coexpress the pan-autonomic determinantPaired-like homeodomain 2b(Phox2b) together with markers of Schwann cell precursors. Some give rise to Schwann cells after down-regulation of PHOX2b. Others form parasympathetic ganglia after being guided to the site of ganglion formation by the nerves that carry preganglionic fibers, a parsimonious way of wiring the pathway. Thus, cranial Schwann cell precursors are the source of parasympathetic neurons during normal development.


1967 ◽  
Vol 32 (2) ◽  
pp. 497-518 ◽  
Author(s):  
Edmund B. Masurovsky ◽  
Mary Bartlett Bunge ◽  
Richard P. Bunge

Under suitable conditions rat dorsal root ganglia differentiate and myelinate in culture, providing an organotypic model of the ganglion (8). Mature cultures of this type were irradiated with a 40 kR dose of 184 kvp X-rays and, after daily observation in the living state, were fixed for light and electron microscopy. Within 24 hr after irradiation, numerous Schwann cells investing unmyelinated axons acutely degenerate. The axons thus denuded display little change. Conversely, few ultrastructural changes develop in Schwann cells investing myelinated axons until after the 4th day. During the 4–14 day period, these Schwann cells and their related myelin sheaths undergo progressive deterioration. Associated axons decrease in diameter but are usually maintained. Myelin deterioration begins as a nodal lengthening and then progresses along two different routes. In intact Schwann cells, fragmentation of myelin begins in a pattern reminiscent of Wallerian degeneration, but its slow breakdown thereafter suggests metabolic disturbances in these Schwann cells. The second pattern of myelin deterioration, occurring after complete degeneration of the related Schwann cell, involves unusual configurational changes in the myelin lamellae. Atypical repeating periods are formed by systematic splitting of lamellae at each major dense line with further splitting at the intraperiod line (Type I) or by splitting in the region of every other intraperiod line (Type II); some sheaths display a compact, wavy, inner zone and an abnormally widened lamellar spacing peripherally (Type III). Extensive blebbing of myelin remnants characterizes the final stages of this extracellular myelin degradation. These observations provide the first description of ultrastructural changes produced by ionizing radiation in nerve fascicles in vitro.


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