Abstract
Brains undergo significant remodeling after traumatic brain injury (TBI). The Rho guanine triphosphate (GTP)ase pathways control brain remodeling during development and under pathological conditions. How the Rho GTPase pathways are regulated in the brain after TBI remains largely unknown, however. This study used the rat fluid percussion injury model to investigate changes in the Rho GTPase pathways after TBI. The results showed that TBI leads to activation and translocation of RhoA and Rac1 proteins from cytosolic fraction to the membrane fraction after injury. Consistently, the Rho guanine nucleotide exchange factors GEF-H1 and Cool-2/αPix are significantly activated by dephosphorylation and accumulation in the cytosolic fractions during the post-TBI phase. Because the Rho GTPase pathways are key regulators of brain remodeling, these results depict regulatory mechanisms of the Rho GTPase pathways after TBI, and pave the way for the study of therapeutic agents targeting the Rho GTPase pathways for functional recovery after TBI.
| Original language | English |
|---|---|
| Pages (from-to) | 1449-1456 |
| Number of pages | 8 |
| Journal | Journal of Neurotrauma |
| Volume | 30 |
| Issue number | 16 |
| DOIs | |
| State | Published - Aug 15 2013 |
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Keywords
- brain remodeling
- Cool2/αPix
- GEF-H1
- Rho GTPases
- traumatic brain injury
ASJC Scopus subject areas
- Clinical Neurology
Cite this
Changes in the GEF-H1 pathways after traumatic brain injury. / Sabirzhanova, Inna; Liu, Chunli; Zhao, Jingwei; Bramlett, Helen; Dalton Dietrich, W.; Hu, Bingren.
In: Journal of Neurotrauma, Vol. 30, No. 16, 15.08.2013, p. 1449-1456.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Changes in the GEF-H1 pathways after traumatic brain injury
AU - Sabirzhanova, Inna
AU - Liu, Chunli
AU - Zhao, Jingwei
AU - Bramlett, Helen
AU - Dalton Dietrich, W.
AU - Hu, Bingren
PY - 2013/8/15
Y1 - 2013/8/15
N2 - Brains undergo significant remodeling after traumatic brain injury (TBI). The Rho guanine triphosphate (GTP)ase pathways control brain remodeling during development and under pathological conditions. How the Rho GTPase pathways are regulated in the brain after TBI remains largely unknown, however. This study used the rat fluid percussion injury model to investigate changes in the Rho GTPase pathways after TBI. The results showed that TBI leads to activation and translocation of RhoA and Rac1 proteins from cytosolic fraction to the membrane fraction after injury. Consistently, the Rho guanine nucleotide exchange factors GEF-H1 and Cool-2/αPix are significantly activated by dephosphorylation and accumulation in the cytosolic fractions during the post-TBI phase. Because the Rho GTPase pathways are key regulators of brain remodeling, these results depict regulatory mechanisms of the Rho GTPase pathways after TBI, and pave the way for the study of therapeutic agents targeting the Rho GTPase pathways for functional recovery after TBI.
AB - Brains undergo significant remodeling after traumatic brain injury (TBI). The Rho guanine triphosphate (GTP)ase pathways control brain remodeling during development and under pathological conditions. How the Rho GTPase pathways are regulated in the brain after TBI remains largely unknown, however. This study used the rat fluid percussion injury model to investigate changes in the Rho GTPase pathways after TBI. The results showed that TBI leads to activation and translocation of RhoA and Rac1 proteins from cytosolic fraction to the membrane fraction after injury. Consistently, the Rho guanine nucleotide exchange factors GEF-H1 and Cool-2/αPix are significantly activated by dephosphorylation and accumulation in the cytosolic fractions during the post-TBI phase. Because the Rho GTPase pathways are key regulators of brain remodeling, these results depict regulatory mechanisms of the Rho GTPase pathways after TBI, and pave the way for the study of therapeutic agents targeting the Rho GTPase pathways for functional recovery after TBI.
KW - brain remodeling
KW - Cool2/αPix
KW - GEF-H1
KW - Rho GTPases
KW - traumatic brain injury
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U2 - 10.1089/neu.2012.2673
DO - 10.1089/neu.2012.2673
M3 - Article
C2 - 23611588
AN - SCOPUS:84881410704
VL - 30
SP - 1449
EP - 1456
JO - Journal of Neurotrauma
JF - Journal of Neurotrauma
SN - 0897-7151
IS - 16
ER -