Premium
Number of oligodendrocyte progenitors recruited to the lesioned spinal cord is modulated by the levels of the cell cycle regulatory protein p27Kip‐1
Author(s) -
Crockett David P.,
Burshteyn Mark,
Garcia Corina,
Muggironi Michela,
CasacciaBonnefil Patrizia
Publication year - 2004
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20111
Subject(s) - remyelination , biology , oligodendrocyte , cell cycle , bromodeoxyuridine , spinal cord , progenitor cell , spinal cord injury , neuroscience , lesion , immunology , microbiology and biotechnology , cell , myelin , pathology , central nervous system , stem cell , medicine , immunohistochemistry , genetics
Remyelination is a critical step for recovery of function after demyelination and defines the ability to generate new myelin. This repair process is dependent on the presence of resident oligodendrocyte progenitors (OLPs) that have been shown to remyelinate axons after demyelination. We have previously shown that the levels of the cell cycle inhibitor p27Kip‐1 modulate the number of neonatal cortical OLPs. We now asked whether this cell cycle molecule plays also a role in regulating the number of adult OLP in the spinal cord after demyelination induced by lysolecithin injection. The proliferative response of OLP in the spinal cord of injected wild‐type (wt) and p27Kip‐1 null mice was evaluated 3 days after lesion. In vivo labeling with bromodeoxyuridine (BrdU) was used to identify cells in S phase. Double immunofluorescence for the OLP marker NG2, and for BrdU was used to count the number of proliferating progenitors. Consistent with a role of p27Kip‐1 in regulating the number of adult OLP in the injured spinal cord, a larger number of proliferating OLPs was observed in p27Kip‐1null mice compared with wild‐type controls. These cells were able to differentiate as assessed by the presence of MBP + cells in the spinal cord 14 days after injury. We conclude that the cellular levels of the cell cycle inhibitor p27Kip‐1 modulate the repair response of OLPs to injury in the adult spinal cord. © 2004 Wiley‐Liss, Inc.