scholarly journals pEGFR promotes the neural function recovery after decompression of compressed spinal cord injury

2019 ◽  
Author(s):  
Rui Gong ◽  
Min Zhang ◽  
Kexin Sun ◽  
Wei Qi ◽  
Shanquan Sun ◽  
...  

Abstract Purpose Investigating the roles of phosphorylated epidermal growth factor receptor (pEGFR) in the recovery of neural function after decompression of CSCI, therefore provide experimental basis for the development of therapeutic strategies and medicines for treating CSCI. Methods A CSCI model was established with a customized device, and was then subjected to spinal decompression. The motor functions were monitored by the Basso, Beattie & Bresnahan(BBB) locomotor rating scale; the number of axonal myelinated fibers was estimated by staining with luxol fast blue (LFB); pEGFR and phosphorylated Akt1 (pAkt1) were detected by Western blot; pEGFR+-NG2+(NG2+ cells are precursor to oligodendrocytes and pAkt1+-NG2+ cells were detected by double-labeling immunefluorescence assay. Results After decompression of CSCI, the BBB scores and the number of myelinated nerve fibers gradually increased with time. Meanwhile, the expression of pEGFR and pAkt1 were up-regulated and the number of pEGFR+-NG2+ and pAkt1+-NG2+ cells increased consistent with the changes of motor functions and the number of myelinated nerve fibers. Whereas, significant decreases in BBB scores, expression level of pAkt1, as well as numbers of myelinated nerve fibers, and pAkt1+-NG2+ cells were observed after inhibition of expression. Conclusions Up-regulated expression of pEGFR can promote recovery of neurological functions in rats with CSCI. This effect is achieved by activation of pAkt1(a downstream signal molecule of pEGFR), which subsequently promotes the proliferation of oligodendrocyte precursor cells (OPCs).

1953 ◽  
Vol 98 (3) ◽  
pp. 269-276 ◽  
Author(s):  
E. De Robertis ◽  
C. M. Franchi

A technique has been developed for the extrusion of axon material from myelinated nerve fibers. This material is then compressed and prepared for observation with the electron microscope. All the stages of preparation and purification of the axon material can be checked microscopically and in the present paper they are illustrated with phase contrast photomicrographs. Observation with the electron microscope of the compressed axons showed the presence of the following components: granules, fibrils, and a membranous material. Only the larger granules could be seen with the ordinary microscope. A considerable number of dense granules were observed. Of these the largest resemble typical mitochondria of 250 mµ by 900 mµ. In addition rows or small clusters of dense granules ranging in diameter from 250 to 90 mµ were present. In several specimens fragments of a membrane 120 to 140 A thick and intimately connected with the axon were found. The entire axon appeared to be constituted of a large bundle of parallel tightly packed fibrils among which the granules are interspersed. The fibrils are of indefinite length and generally smooth. They are rather labile structures, less resistant in the rat than in the toad nerve. They varied between 100 and 400 A in diameter and in some cases disintegrated into very fine filaments (less than 100 A thick). The significance is discussed of the submicroscopic structures revealed by electron microscopy of the material prepared in the way described.


2016 ◽  
Vol 14 (7) ◽  
pp. 3345-3350 ◽  
Author(s):  
Alvaro Gabriel Piza ◽  
Fernando Daniel Farfan ◽  
Ana Lia Albarracin ◽  
Facundo Adrian Lucianna ◽  
Jorge Humberto Soletta ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jeanette M. Metzger ◽  
Helen N. Matsoff ◽  
Don Vu ◽  
Alexandra D. Zinnen ◽  
Kathryn M. Jones ◽  
...  

Minimal myelination is proposed to be a contributing factor to the preferential nigral neuronal loss in Parkinson’s disease (PD). Similar to nigral dopaminergic neurons, sympathetic neurons innervating the heart have long, thin axons which are unmyelinated or minimally myelinated. Interestingly, cardiac sympathetic loss in PD is heterogeneous across the heart, yet the spatial relationship between myelination and neurodegeneration is unknown. Here, we report the mapping of myelin basic protein (MBP) expression across the left ventricle of normal rhesus macaques (n = 5) and animals intoxicated with systemic 6-OHDA (50 mg/kg iv) to model parkinsonian cardiac neurodegeneration (n = 10). A subset of 6-OHDA-treated rhesus received daily dosing of pioglitazone (5 mg/kg po; n = 5), a PPARγ agonist with neuroprotective properties. In normal animals, MBP-immunoreactivity (-ir) was identified surrounding approximately 14% of axonal fibers within nerve bundles of the left ventricle, with more myelinated nerve fibers at the base level of the left ventricle than the apex p < 0.014 . Greater MBP-ir at the base was related to a greater number of nerve bundles at that level relative to the apex p < 0.05 , as the percent of myelinated nerve fibers in bundles was not significantly different between levels of the heart. Cardiac sympathetic loss following 6-OHDA was associated with decreased MBP-ir in cardiac nerve bundles, with the percent decrease of MBP-ir greater in the apex (84.5%) than the base (52.0%). Interestingly, cardiac regions and levels with more MBP-ir in normal animals showed attenuated sympathetic loss relative to areas with less MBP-ir in 6-OHDA + placebo (r = −0.7, p < 0.014 ), but not in 6-OHDA + pioglitazone (r = −0.1) subjects. Our results demonstrate that myelination is present around a minority of left ventricle nerve bundle fibers, is heterogeneously distributed in the heart of rhesus macaques, and has a complex relationship with cardiac sympathetic neurodegeneration and neuroprotection.


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