[Role of endoplasmic reticulum stress during myocardial apoptosis in rats with severe burn injury].
OBJECTIVE
Endoplasmic reticulum stress (ERS) mediated apoptosis is one of the eukaryotic cellular apoptotic pathways, to investigate the potential role of ERS during myocardium apoptosis in rats with severe burn injury.


METHODS
Sixty-four 7-week-old male Wistar rats, weighing 200-220 g, were randomly divided into 2 groups. Thirty percentage of total body surface area full-thickness thermal injury was produced in 32 rats of burn group, while sham burn was produced in 32 rats of control group. The heart tissues were harvested from 8 rats in each group at 1, 4, 7, and 14 days after burn to observe the changes of myocardium ultrastructure with transmission electron microscope (TEM). Myocardium apoptosis was detected with TUNEL assay. The expressions of glucose regulated protein 78 (GRP 78), C/EBP-homologous protein (CHOP), and cleaved Caspase 12 in different pathways of ERS were analysed with Western blot.


RESULTS
All rats survived during the experiment. Apoptotic changes of cardiomyocytes were observed in burn group, and the apoptosis index in burn group was significantly higher than that in control group at each time point (P < 0.05), and it reached peak at 7 days after burn injury (P < 0.05). The expressions of myocardial GRP 78, CHOP, and cleaved Caspase 12 showed persistent elevation in burn group. The expressions of GRP 78 and cleaved Caspase 12 in burn group were significantly higher than those in control group at each time point (P < 0.05), while the expression of CHOP was higher than that in control group at the other time points (P < 0.05) except 1st day after burn injury.


CONCLUSIONS
ERS and CHOP, Caspase 12 mediated apoptotic pathway are activated in myocardium after severe burn injury, and this may be one pathway of myocardium apoptosis.
Department of Burns & Plastic, First Affiliated Hospital of General Hospital of Chinese PLA, Beijing 100048, PR China.
Wanli
W
Chu
Jiake
J
Chai
Yongqiang
Y
Feng
Li
L
Ma
Chao
C
Hu
D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D002056:Burns / Q000378:metabolism* / Q000473:pathology; D053454:Caspase 12 / Q000378:metabolism; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress; D006360:Heat-Shock Proteins / Q000378:metabolism; D008297:Male; D046529:Microscopy, Electron, Transmission; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D051742:Transcription Factor CHOP / Q000378:metabolism; D000091342:Endoplasmic Reticulum Chaperone BiP
D053454:Caspase 12; D006360:Heat-Shock Proteins; D051742:Transcription Factor CHOP; C497251:Ddit3 protein, rat; C051684:GRP78 protein, rat; D000091342:Endoplasmic Reticulum Chaperone BiP; C506443:Casp12 protein, rat