EXPRESSION OF ENDOPEPTIDASE-24.11 (COMMON ACUTE LYMPHOBLASTIC-LEUKEMIA ANTIGEN CD10) IN THE SCIATIC-NERVE OF THE ADULT-RAT AFTER LESION ANDDURING REGENERATION
C. Kioussi et al., EXPRESSION OF ENDOPEPTIDASE-24.11 (COMMON ACUTE LYMPHOBLASTIC-LEUKEMIA ANTIGEN CD10) IN THE SCIATIC-NERVE OF THE ADULT-RAT AFTER LESION ANDDURING REGENERATION, European journal of neuroscience, 7(5), 1995, pp. 951-961
Endopeptidase-24.11, which is identical with the common acute lymphobl
astic leukaemia antigen CD10 (CALLA), is a cell surface Zn2+ metallopr
otease that regulates peptide-induced responses in different tissues,
including the nervous and immune systems. In the peripheral nervous sy
stem, 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 o
f the adult rat sciatic nerve on the expression of the endopeptidase b
y Schwann cells in situ. Endopeptidase-24.11 was monitored by immunocy
tochemistry using the monoclonal anti-endopeptidase antibody 23B11. Fo
r comparison, a parallel study was carried out with a monoclonal antib
ody directed against the rat nerve growth factor receptor. We found th
at (i) all Schwann cells of the distal segment re-expressed endopeptid
ase-24.11 as early as 4 days after axotomy, the level of immunostainin
g reaching a maximum after 2 weeks, (ii) axonal regeneration repressed
Schwann cell expression of endopeptidase-24.11, and (iii) the inducti
on of the nerve growth factor receptor followed a similar pattern to t
hat of endopeptidase-24.11 in the transected and crushed nerve. Enzyma
tic amplification of endopeptidase-24.11 cDNA from normal and axotomiz
ed adult rat sciatic nerve confirmed the expression of endopeptidase-2
4.11 in these tissues. Our results show that the expression of endopep
tidase-24.11 in Schwann cells, as is the case with the nerve growth fa
ctor receptor, is induced by the loss of the normal axon-Schwann cell
contact. The significant increase in the expression of endopeptidase-2
4.11 by Schwann cells after axonal damage suggests that the enzyme cou
ld play a role in axonal regeneration.