Acute spinal cord injury in rats induces autophagy activation.
OBJECTIVE
Autophagy is an important process that balances cellular protein synthesis and degradation and is involved in many physiological and pathological conditions. However, the precise role of autophagy has not yet been defined in the model of spinal cord injury (SCI).


METHODS
Here, we utilized a hemisection model of acute SCI to elucidate the role of autophagy in the pathological processes underlying SCI.


RESULTS
LC3B-II, a well-known marker of autophagy, was immunohistochemically detected 4H after SCI, peaked at 3D, and decreased at 21D. Hematoxylin-eosin (HE) staining confirmed accurate spinal cord hemisection, which was accompanied by both neuronal swelling and shrunken neurons with darkly stained, condensed nuclei. These findings suggest that the process of autophagy is related with pathological changes following SCI.


CONCLUSIONS
Our results indicate autophagy is involved in the pathological changes after SCI, and potential therapies to promote neuronal regeneration following SCI should target the mechanism of autophagy.
Chinese PLA General Hospital, Department of Orthopedics, Beijing, P.R. China.
Hongping
H
Hou
Lihai
L
Zhang
Licheng
L
Zhang
Daohong
D
Liu
Zhi
Z
Mao
Hailong
H
DU
Peifu
P
Tang
D000818:Animals; D001343:Autophagy / Q000502:physiology*; D007150:Immunohistochemistry; D007796:Laminectomy; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000378:metabolism / Q000473:pathology*
C502070:MAP1LC3B protein, human; D008869:Microtubule-Associated Proteins