Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acidic protein in maintenance of pain behaviors [corrected].
Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acidic protein in maintenance of pain behaviors [corrected].
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DOI：
10.1016/j.pain.2009.02.006
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发表时间：
2009-05
期刊：
影响因子：
7.4
通讯作者：
Luo ZD
中科院分区：
文献类型：
--
作者：
Kim DS;Figueroa KW;Li KW;Boroujerdi A;Yolo T;Luo ZD
To explore cellular changes in sensory neurons after nerve injury and identify potential target genes contributing to different stages of neuropathic pain development, we used Affymetrix oligo arrays to profile gene expression patterns in L5/6 dorsal root ganglia (DRG) from the neuropathic pain model of left L5/6 spinal nerve ligation at different stages of neuropathic pain development. Our data indicated that nerve injury induced changes in expression of genes with similar biological functions in a temporal specific manner that correlates with particular stages of neuropathic pain development, indicating dynamic neuroplasticity in the DRG in response to peripheral nerve injury and during neuropathic pain development. Data from post-array validation indicated that there was a temporal correlation between injury-induced expression of the glial fibrillary acidic protein (GFAP), a marker for activated astrocytes, and neuropathic pain development. Spinal nerve ligation injury in GFAP knockout mice resulted in neuropathic pain states with similar onset, but a shortened duration compared with that in age, and gender-matched wild-type littermates. Intrathecal GFAP antisense oligonucleotide treatment in injured rats with neuropathic pain states reversed injury-induced behavioral hypersensitivity and GFAP upregulation in DRG and spinal cord. Together, these findings indicate that injury-induced GFAP upregulation not only serves as a marker for astrocyte activation, but it may play a critical, but yet identified, role in the maintenance of neuropathic pain states.
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影响因子：
4.2
作者：
FEINSTEIN, DL;WEINMASTER, GA;MILNER, RJ
通讯作者：
MILNER, RJ
影响因子：
2.5
作者：
HAJOS, F;CSILLIK, B;KNYIHARCSILLIK, E
通讯作者：
KNYIHARCSILLIK, E
影响因子：
3.3
作者：
ENG, LF
通讯作者：
ENG, LF
DOI：
10.1073/pnas.91.26.12540
发表时间：
1994-12-20
影响因子：
11.1
作者：
JI, RR;ZHANG, Q;HOKFELT, T
通讯作者：
HOKFELT, T
影响因子：
3.3
作者：
Honore, P;Rogers, SD;Mantyh, PW
通讯作者：
Mantyh, PW