[Changes in proliferative activity of myoblasts and expression of Akt in skeletal muscle of rats after severe burn injury].
OBJECTIVE
To investigate changes in proliferative activity of myoblasts in skeletal muscle and potential role of phosphorylated Akt on it, so that a better understanding in mechanisms of skeletal muscle atrophy after burn injury will be got.


METHODS
One hundred and twenty Wistar rats were randomly divided into 2 groups: control and severe thermal injury group. Rats in severe thermal injury group were subjected to a 40% total body surface area full-thickness scald injury, and Tibialis Anterior (TA) muscles were collected on 0, 1, 4, 7, 10, 14 days post-injury. After muscle mass determined, immunohistochemical double staining was used for detection of Proliferative Cell Nuclear Antigen (PCNA) of myoblasts. Protein expression of total Akt and phosphorylated Akt was determined by Western Blot.


RESULTS
Burn injury induced significant reduction of TA muscle mass and maximal reduction of it appeared by 4 days after injury (P < 0.01). Proliferative activity of myoblasts decreased significantly from the first day post-injury (P < 0.01) and increased slowly to basal level of controls after 7 days post-injury. The phosphorylated Akt was undetectable in both of controls and injured samples before 4 days but increased significantly after 7 days post-injury (P < 0.01), though total Akt expression had no significant alteration at any time points (P > 0.05).


CONCLUSIONS
Decrease in proliferative activity of myoblasts may be one of the contributors of significant atrophy of skeletal muscle after burn injury. Effect of phosphorylated Akt on proliferation attenuated in early stage and increased significantly in later stage after burn injury may partly explain the changes in proliferative activity of myoblasts.
Duan
Hong-jie
HJ
Burns Institute, First Hospital, Affiliated to the Chinese PLA General Hospital, Beijing 100048, China.
Chai
Jia-ke
JK
Sheng
Zhi-yong
ZY
Liang
Li-ming
LM
Yin
Hui-nan
HN
Shen
Chuan-an
CA
D000818:Animals; D002056:Burns / Q000378:metabolism / Q000473:pathology*; D049109:Cell Proliferation; D004195:Disease Models, Animal; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology*; D032446:Myoblasts / Q000378:metabolism / Q000473:pathology*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
C494920:Akt1 protein, rat; D051057:Proto-Oncogene Proteins c-akt