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. 2012 Sep 15;7(26):2005-11.
doi: 10.3969/j.issn.1673-5374.2012.26.001.

P75 and phosphorylated c-Jun are differentially regulated in spinal motoneurons following axotomy in rats

Qiuju Yuan  1 , Huanxing Su  2 , Wutian Wu  3 , Zhi-Xiu Lin  1
Affiliations

P75 and phosphorylated c-Jun are differentially regulated in spinal motoneurons following axotomy in rats

Qiuju Yuan et al. Neural Regen Res. .

Abstract

The neurotrophin receptor (p75) activates the c-Jun N-terminal kinase (JNK) pathway. Activation of JNK and its substrate c-Jun can cause apoptosis. Here we evaluate the role of p75 in spinal motoneurons by comparing immunoreactivity for p75 and phosphorylated c-Jun (p-c-Jun), the production of JNK activation in axotomized motoneurons in postnatal day (PN)1, PN7, PN14 and adult rats. Intensive p-c-Jun was induced in axotomized motoneurons in PN1 and PN7. In PN14, p-c-Jun expression was sharply reduced after the same injury. The decreased expression of p-c-Jun at this age coincided with a developmental switch of re-expression of p75 in axotomized cells. In adult animals, no p-c-Jun but intensive p75 was detected in axotomized motoneurons. These results indicate differential expression or turnover of phosphorylation of c-Jun and p75 in immature versus mature spinal motoneurons in response to axonal injury. The non-co-occurrence of p75 and p-c-Jun in injured motoneurons indicated that p75 may not activate JNK pathway, suggesting that the p75 may not be involved in cell death in axotomized motoneurons.

Keywords: adult; apoptosis; axonal regeneration; axotomy; c-Jun N-terminal kinase; motoneuron; neonatal; nerve growth factor receptor; spinal cord; transcription factor.

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Conflict of interest statement

Conflicts of interest: None declared.

Figures

Figure 1
Figure 1
Photomicrographs of neutral red stained transverse sections of nonlesioned (A, C, E, G) and lesioned side (B, D, F, H) of the C7 spinal cord of postnatal day (PN)1 (A, B), PN7 (C, D), PN14 (E, F) and adult (G, H) rats at 1 week following distal axotomy. Few motoneurons are found in the ventral horn of the lesion side spinal cord in PN1 (B) and PN7 (D) compared with their normal control (A, C, respectively). Many motoneurons are found in the lesioned side of PN14 (F) and adult (H) rats, which is comparable to their normal control (E, G, respectively). Scale bar: 200 μm. Quantitative analysis of axotomized motoneuron survival showed that distal axotomy induced massive motoneuron loss in PN1 and PN7 rats. In contrast, distal axotomy did not induce significant motoneuron loss in PN14 and adult rats at 1 week post-lesion (I). Data are expressed as a percentage (mean ± SEM) of the contralateral (normal) cell numbers.
Figure 2
Figure 2
Photomicrographs of transverse sections of nonlesioned (A, B, C) and lesioned sides of the C7 spinal cord of postnatal (PN)1 (D, E, F), PN7 (G, H, I), PN14 (J, K, L) and adult (M, N, O) rats stained with p75 (A, D, G, J, M), c-Jun 63 (B, E, H, K, N) and c-Jun 73 (C, F, I, L, O) at 3 days following distal axotomy. Scale bar: 200 μm. No positive signals for p75 (A), c-Jun 63 (B) and c-Jun 73 (C) could be found in normal spinal cord. Intensive c-Jun 63 (E, H) and c-Jun 73 (F, I) was observed in PN1 (E, F) and PN7 (H, I) rats at 3 days following the injury. Weak c-Jun 63 (K) and c-Jun 73 (L) was seen in PN14 rats. No c-Jun 63 (N) and c-Jun 73 (O) was seen in adult rats. In contrast, no p75 positive signals could be found in PN1 (D) and PN7 (G) rats. In contrast, intensive p75 positive signals were found in PN14 rats (J) and adult rats (M).
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References

    1. Roux PP, Barker PA. Neurotrophin signaling through the p75 neurotrophin receptor. Prog Neurobiol. 2002;67:203–233. - PubMed
    1. Bui NT, Konig HG, Culmsee C, et al. p75 neurotrophin receptor is required for constitutive and NGF-induced survival signalling in PC12 cells and rat hippocampal neurones. J Neurochem. 2002;81:594–605. - PubMed
    1. Barker PA. p75NTR: A study in contrasts. Cell Death Differ. 1998;5:346–356. - PubMed
    1. Fobian K, Owczarek S, Budtz C, et al. Peptides derived from the solvent-exposed loops 3 and 4 of BDNF bind TrkB and p75(NTR) receptors and stimulate neurite outgrowth and survival. J Neurosci Res. 2010;88:1170–1181. - PubMed
    1. Bachis A, Avdoshina V, Zecca L, et al. Human immunodeficiency virus type 1 alters brain-derived neurotrophic factor processing in neurons. J Neurosci. 2012;32:9477–9484. - PMC - PubMed