Expression of discoidin domain receptor 2 in different phases of alcoholic liver fibrosis in a rat model.
- Author:
Hui-min LIU
1
;
Ming YAN
;
Xi-hong ZHANG
;
Li LIU
;
Nan SHANG
;
Hai-tao ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Collagen; metabolism; Discoidin Domain Receptors; Disease Models, Animal; Liver Cirrhosis, Alcoholic; metabolism; pathology; Male; Rats; Rats, Wistar; Receptor Protein-Tyrosine Kinases; metabolism; Receptors, Mitogen; metabolism
- From: Chinese Journal of Hepatology 2008;16(6):425-429
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the expressions of discoidin domain receptor 2 (DDR2) in different phases of alcoholic liver fibrosis (ALF) in a rat model and to study the possible association between DDR2 and collagen deposition in ALF.
METHODSAfter an ALF rat model was established by alcohol gastrogavage and an olive oil diet, the liver histopathology was observed in different phases of the development of fibrosis. The expressions of DDR2 mRNA and protein were also detected by RT-PCR and Western blot respectively to make a dependability analysis with the index of ALF.
RESULTS(1) The expressions of DDR2 mRNA and protein increased gradually along with ALF aggravation. In the normal control group, they were respectively 1.023+/-0.132 and 0.321+/-0.027; in the model 1 group (week 12) they were 3.644+/-1.686, 0.476+/-0.046; in the model 2 group (week 16) they were 8.337+/-2.387, 0.738+/-0.057; and in the model 3 group (week 20) they were 15.730+/-4.569, 0.997+/-0.049. The differences of DDR2 mRNA (F = 21.74, P less than 0.01) and protein (F = 10.38, P less than 0.01) among these four groups were significant. (2) The expressions of DDR2 had a positive correlation with collagen type I, III, IV contents and the serum index of ALF, especially with type III and IV collagen and serum hexadecenoic acid.
CONCLUSIONThe expression of DDR2 in this ALF model correlates closely with collagen deposition in the liver, suggesting that it may play an important role in ALF pathogenesis.