EXPRESSION OF ENDOPEPTIDASE-24.11 (COMMON ACUTE LYMPHOBLASTIC-LEUKEMIA ANTIGEN CD10) IN THE SCIATIC-NERVE OF THE ADULT-RAT AFTER LESION AND DURING REGENERATION
EXPRESSION OF ENDOPEPTIDASE-24.11 (COMMON ACUTE LYMPHOBLASTIC-LEUKEMIA ANTIGEN CD10) IN THE SCIATIC-NERVE OF THE ADULT-RAT AFTER LESION AND DURING REGENERATION
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DOI：
10.1111/j.1460-9568.1995.tb01083.x
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发表时间：
1995-05-01
影响因子：
3.4
通讯作者：
MATSAS, R
中科院分区：
文献类型：
--
作者：
KIOUSSI, C;MAMALAKI, A;MATSAS, R
内肽酶-24.11与常见的急性淋巴细胞白血病抗原CD 10（CALLA）相同，是一种细胞表面Zn 2+金属蛋白酶，可调节不同组织（包括神经和免疫系统）中的肽诱导反应。在周围神经系统中，高水平的酶存在于所有新生儿和出生后早期的许旺细胞中，而随着髓鞘形成的进行，它在大多数形成髓鞘的细胞中逐渐受到抑制，但保留在成年动物的非髓鞘形成细胞中。在本研究中，我们研究了成年大鼠坐骨神经横断，挤压和再生的影响，在原位雪旺细胞表达的内肽酶。使用单克隆抗内肽酶抗体23 B11通过免疫细胞化学监测内肽酶-24.11。为了比较，用针对大鼠神经生长因子受体的单克隆抗体进行平行研究。我们发现：（i）所有远段雪旺细胞早在轴突切断后4天就重新表达内肽酶-24.11，免疫染色水平在2周后达到最大值，（ii）轴突再生抑制了雪旺细胞内肽酶-24.11的表达，和（iii）神经生长因子受体的诱导遵循与内肽酶-24.11在横断和压碎的神经中的诱导相似的模式。从正常和轴突切断的成年大鼠坐骨神经的内肽酶-24.11 cDNA的酶扩增证实了内肽酶-24.11在这些组织中的表达。我们的研究结果表明，表达内肽酶-24.11在雪旺细胞，是与神经生长因子受体的情况下，是由正常轴突雪旺细胞接触的损失。轴突损伤后雪旺细胞内肽酶-24.11的表达显著增加，表明该酶可能在轴突再生中发挥作用。
Endopeptidase-24.11, which is identical with the common acute lymphoblastic leukaemia antigen CD10 (CALLA), is a cell surface Zn2+ metalloprotease that regulates peptide-induced responses in different tissues, including the nervous and immune systems. In the peripheral nervous system, high levels of the enzyme are present in all neonatal and early postnatal Schwann cells, while as myelination proceeds it is gradually suppressed in the majority of cells that form myelin but retained in non-myelin-forming cells in the adult animal. In the present study we have investigated the effects of transection, crush and regeneration of the adult rat sciatic nerve on the expression of the endopeptidase by Schwann cells in situ. Endopeptidase-24.11 was monitored by immunocytochemistry using the monoclonal anti-endopeptidase antibody 23B11. For comparison, a parallel study was carried out with a monoclonal antibody directed against the rat nerve growth factor receptor. We found that (i) all Schwann cells of the distal segment re-expressed endopeptidase-24.11 as early as 4 days after axotomy, the level of immunostaining reaching a maximum after 2 weeks, (ii) axonal regeneration repressed Schwann cell expression of endopeptidase-24.11, and (iii) the induction of the nerve growth factor receptor followed a similar pattern to that of endopeptidase-24.11 in the transected and crushed nerve. Enzymatic amplification of endopeptidase-24.11 cDNA from normal and axotomized adult rat sciatic nerve confirmed the expression of endopeptidase-24.11 in these tissues. Our results show that the expression of endopeptidase-24.11 in Schwann cells, as is the case with the nerve growth factor receptor, is induced by the loss of the normal axon-Schwann cell contact. The significant increase in the expression of endopeptidase-24.11 by Schwann cells after axonal damage suggests that the enzyme could play a role in axonal regeneration.