Sf. Tzeng et al., Upregulation of the HLH Id gene family in neural progenitors and glial cells of the rat spinal cord following contusion injury, J NEUROSC R, 66(6), 2001, pp. 1161-1172
Spinal cord injury (SCI) leads to a complex sequence of cellular responses,
including astrocyte activation, oligodendrocyte death, and ependymal cell
proliferation. Inhibitors of DNA binding (Id1, Id2, ld3) belong to a helix-
loop-helix (HLH) gene family. ld genes have been implicated in playing a vi
tal role in the proliferation of many cell types, including astrocytes and
myoblasts. In the present study, the expression of Id family members in spi
nal cord after contusion injury was investigated by in situ hybridization.
Id1, Id2, and ld3 mRNA expression was upregulated 5 mm rostral and caudal t
o the lesion center, and reached maximal levels 3 days after SCI. In additi
on, cell populations expressing Id1, Id2, and ld3 mRNA were maximally incre
ased 3 days after SCI. The increase in Id2 and ld3 mRNA expression and Id2
and ld3 mRNA+ cells was still observed at 8 days. The Id mRNA expressing ce
lls were phenotyped by combining immunostaining of cell-specific markers wi
th in situ hybridization. Glial fibrillary acidic protein (GFAP)+ astrocyte
s were found to express all three ld mRNA, whereas S-100 alpha+ astrocytes
only expressed high levels of Id2 and ld3 mRNA. Cells having a neural proge
nitor morphology and the marker nestin appeared after SCI and they expresse
d Id1, Id2, and Id3 mRNA. Interestingly, some Rip+ oligodendrocytes located
in the areas close to the central canal expressed Id3 mRNA after injury. I
n conclusion, Id genes are upregulated in a time-dependent manner in astroc
ytes, oligodendrocytes, and neural progenitor subpopulations after SCl, sug
gesting that they play major roles in cellular responses following SCI. (C)
2001 Wiley-Liss, Inc.