Non-neuronal cells are not the limiting factor for the low axonal regeneration in C57BL/6J mice

Oliveira, Alexandre Leite Rodrigues de; Langone, Francesco

doi:10.1590/s0100-879x2000001200011

Cited by 4 publications

(6 citation statements)

References 36 publications

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“…The facts reported above are in line with other works dealing with various isogenic strains of mice showing variations in the regenerative capacity after crushing or sectioning of the sciatic nerve (Lainetti et al, 1995;Lu et al, 1994;Oliveira and Langone, 2000;Oliveira, 2001;Xin et al, 1990). In this sense, C57BL/6J number of regenerated axons, 2 weeks after axotomy, was one-fifth of that in A/J.…”

Section: Introductionsupporting

confidence: 90%

“…In a subsequent study, the genetic and biological nature of such deficiency was linked to multiple loci (Lu et al, 1994). Another relevant finding, described by Oliveira and Langone (2000) was that non-neuronal cells in the nerve, such as Schwann cells, were not the limiting factor behind the poor regenerative potencial of C57BL/6J mice, which may probably be due to the neuronal response to injury itself. However, no mechanisms have been proposed to explain such differential response to axotomy.…”

Section: Introductionmentioning

confidence: 97%

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MHC I expression and synaptic plasticity in different mice strains after axotomy

Sabha

Emirandetti

Cullheim

et al. 2007

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The success of axonal regeneration has been attributed to a co-operation between the severed neurons and the surrounding environment, including non-neuronal cells and the extracellular matrix. Important differences regarding the regeneration potential after injury have been described among inbred mice strains. To date, there is only limited knowledge of how such variation can be linked with the genetic background. It has recently been demonstrated that MHC class I molecules have an influence on the spinal cord synaptic plasticity elicited by a peripheral lesion, and the regenerative capacity following such a lesion. Therefore, in the present work we compared the MHC I expression after axotomy in three isogenic mice strains, namely C57BL/6J, Balb/cJ, and A/J, and investigated the fine ultrastructure of the synaptic elimination process that follows such lesion. The results show that C57BL/6J mice, that have a comparatively poor regenerative potential, display a lower upregulation of MHC I in the spinal cord, coupled with a slower synaptic stripping. On the other hand, A/J mice, which have been shown to have a stronger axonal regrowth potential, showed a clear upregulation of MHC I and a sharp acute loss of afferents, at 1 week after lesion. Our results suggest that a more prominent expression of MHC I in the first week after lesion may positively influence the regenerative outcome associated with a more effective axonal regrowth.

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Section: Introductionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 97%

MHC I expression and synaptic plasticity in different mice strains after axotomy

Sabha

Emirandetti

Cullheim

et al. 2007

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“…Also, the possible lack of trophic support results in apoptotic neuronal death, which also includes the satellite cells in the DRG. This hypothesis is in agreement with a previous report which showed that if a predegenerated nerve was grafted to the proximal stump, C57BL/ 6J regenerative performance was greatly enhanced (13). Also, if exogenous NGF is administered after sciatic nerve transection, sensory neuron death can be partially reduced (20).…”

supporting

confidence: 92%

“…Although Lu et al (11) proposed that such a defect would be a delay rather than a permanent neuronal impairment, Lainetti et al (12) observed a large percentage of sensitive neuron death four weeks after axotomy. It has been proposed that such neuronal death may be the result of a mismatch in the timing of the neuronal need for trophic substances and their production by the non-neuronal cells in the nerve (13). In this respect, apoptotic mechanisms may be involved, and may be related to the previously described loss of C57BL/6J dorsal root ganglion (DRG) neurons.…”

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confidence: 99%

Apoptosis of sensory neurons and satellite cells after sciatic nerve transection in C57BL/6J mice

Oliveira

2001

Braz J Med Biol Res

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The rate of axonal regeneration, after sciatic nerve lesion in adult C57BL/6J mice, is reduced when compared to other isogenic strains. It was observed that such low regeneration was not due just to a delay, since neuronal death was observed. Two general mechanisms of cell death, apoptosis and necrosis, may be involved. By using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) technique, we demonstrated that a large number of sensory neurons, as well as satellite cells found in the dorsal root ganglia, were intensely labeled, thus indicating that apoptotic mechanisms were involved in the death process. Although almost no labeled neurons or satellite cells were observed one week after transection, a more than ten-fold increase in TUNEL labeling was detected after two weeks. The results obtained with the C57BL/6J strain were compared with those of the A/J strain, which has a much higher peripheral nerve regeneration potential. In A/J mice, almost no labeling of sensory neurons or satellite cells was observed after one or two weeks, indicating the absence of neuronal loss. Our data confirm previous observations that approximately 40% of C57BL/6J sensory neurons die after sciatic nerve transection, and indicate that apoptotic events are involved. Also, our observations reinforce the hypothesis that the low rate of axonal regeneration occurring in C57BL/6J mice may be the result of a mismatch in the timing of the neurons need for neurotrophic substances, and production of the latter by non-neuronal cells in the distal stump. Correspondence

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“…The thickness of the myelin sheath is a direct indicator of functional recovery of the nerve because it denotes the level of physiological activity of Schwann cells. This parameter has been used in several studies to evaluate the evolution of the axonal regenerative process (Levi and Bunge 1994;Oliveira and Langone 2000;Pierucci et al 2008). G-CSF treatment reduced the thickness of the myelin sheath and the diameter of the axons in the two strains studied.…”

Section: Discussionmentioning

confidence: 99%

Granulocyte colony‐stimulating factor (G‐CSF) positive effects on muscle fiber degeneration and gait recovery after nerve lesion in MDX mice

2014

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BackgroundG-CSF has been shown to decrease inflammatory processes and to act positively on the process of peripheral nerve regeneration during the course of muscular dystrophy.AimsThe aims of this study were to investigate the effects of treatment of G-CSF during sciatic nerve regeneration and histological analysis in the soleus muscle in MDX mice.MethodsSix-week-old male MDX mice underwent left sciatic nerve crush and were G-CSF treated at 7 days prior to and 21 days after crush. Ten and twenty-one days after surgery, the mice were euthanized, and the sciatic nerves were processed for immunohistochemistry (anti-p75NTR and anti-neurofilament) and transmission electron microscopy. The soleus muscles were dissected out and processed for H&E staining and subsequent morphologic analysis. Motor function analyses were performed at 7 days prior to and 21 days after sciatic crush using the CatWalk system and the sciatic nerve index.ResultsBoth groups treated with G-CSF showed increased p75NTR and neurofilament expression after sciatic crush. G-CSF treatment decreased the number of degenerated and regenerated muscle fibers, thereby increasing the number of normal muscle fibers.ConclusionsThe reduction in p75NTR and neurofilament indicates a decreased regenerative capacity in MDX mice following a lesion to a peripheral nerve. The reduction in motor function in the crushed group compared with the control groups may reflect the cycles of muscle degeneration/regeneration that occur postnatally. Thus, G-CSF treatment increases motor function in MDX mice. Nevertheless, the decrease in baseline motor function in these mice is not reversed completely by G-CSF.

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Non-neuronal cells are not the limiting factor for the low axonal regeneration in C57BL/6J mice

Cited by 4 publications

References 36 publications

MHC I expression and synaptic plasticity in different mice strains after axotomy

MHC I expression and synaptic plasticity in different mice strains after axotomy

Apoptosis of sensory neurons and satellite cells after sciatic nerve transection in C57BL/6J mice

Granulocyte colony‐stimulating factor (G‐CSF) positive effects on muscle fiber degeneration and gait recovery after nerve lesion in MDX mice

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