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everal distinct cell types in the adult central nervous- t8 o1 B7 b! p6 m, Z9 d
system have been suggested to act as stem or prog-
" K: N7 s2 k. P: P! kenitor cells generating new cells under physiological+ Y( C% S* x4 E5 O$ u1 f2 {
or pathological conditions. We have assessed the% M& d- |- O$ i& _ r7 J
origin of new cells in the adult mouse spinal cord by" l& e- c+ t( k: G4 F' [2 t
genetic fate mapping. Oligodendrocyte progenitors' o- |* }% @0 i9 A! T% E
self-renew, give rise to newmature oligodendrocytes,+ C% ~. v) U, o- z4 t2 V5 _9 A; c
and constitute the dominating proliferating cell popu-9 o7 `2 z0 _2 M- ^% R% H$ ]
lation in the intact adult spinal cord. In contrast, astro-* x! |, R2 r+ o6 v$ f% {! r
cytes and ependymal cells, which are restricted to
- c% C" Q: q! {& p$ \% q& Ilimited self-duplication in the intact spinal cord,7 Z* s1 K+ ?' n+ P( B ~: ^
generate the largest number of cells after spinal cord4 p2 g, u2 s' W7 H8 o% o
injury. Only ependymal cells generate progeny of
( W, Z' D7 z3 U- d# z, t1 n. q6 Fmultiple fates, and neural stemcell activity in the intact
2 z6 F$ _ ^ `and injured adult spinal cord is confined to this cell
3 u k e; J' q, q9 i: Wpopulation. We provide an integrated view of how
5 K) F9 ?4 [& iseveraldistinct cell types contribute in complementary# L% `0 j1 Z; I0 n4 ]: _- ]
ways to cell maintenance and the reaction to injury. |
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