[Expression of transforming growth factor-beta1 and connective tissue growing factor in schistosomal hepatic fibrosis of mice]. 2012

Jia-quan Huang, and Jun Zhu, and Lan Li, and Yun-tao Jiao, and Lei Xu, and Ran Tao, and Xiang-xue Fan, and Ke Ma, and Wei Guo, and Qin Ning
Department of Infectious Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China

OBJECTIVE To establish the model of hepatic fibrosis in mice infected with Schistosoma japonicum and observe the expression of transforming growth factor-beta1 (TGF-beta1) and connective tissue growing factor (CTGF) in mice model. METHODS Thirty BALB/c mice were randomly assigned to control group and model group. Each mouse of model group was infected with (30 +/- 1) S. japonicum cercariae through the abdominal skin. Serum samples were collected at 4, 6, 8, 10, and 12 weeks after infection, and were analyzed for the levels of ALT and AST. Pathological changes and proliferation of hepatic collagen fibers in liver tissue were observed after HE staining and Masson staining. Immunohistochemistry and real-time PCR were used to detect the protein and mRNA expression of CTGF and TGF-pl. RESULTS 6-12 weeks after infection, there was significant difference in ALT and AST between model group and control group (P43.05). At 12th week, ALT [(173.53 +/- 31.12) U/I] and AST [(301.00 +/- 34.87) U/LI in model group were higher than those in control group [(42.00 +/- 3.53) and 96.58 +/- 11.26) U/L] . In model group, egg granulomas formed in the liver, and the formation of hepatic fibrosis was significant in portal areas, and there was tree-like hepatic fibrosis around the portal vein branch. 8 weeks after infection, hepatic fibrosis area in mice of model group increased considerably, and there was significant difference in percentage of positive area of collagen between 12th week [(23.83 +/- 1.68) %] and control group [(1.23 +/- 0.14) %] (P < 0.05). 10 and 12 weeks after infection, the percentage of positive area of TGF-beta1 [(22.34 +/- 2.58)% and (25.82 +/- 3.01) %] and CTGF [(1 l.32 +/- 2.44)% and (14.51 +/- 2.05) %] was higher respectively than that of the control [(2.56 +/- 0.87)%, and (1.09 +/- 0.73)% (P < 0.05). 6, 8, 10, and 12 weeks after infection, both TGF-beta1 and CTGF mRNA increased gradually, higher than that in control group (P < 0.05). 10 weeks after infection, TGF-beta1 mRNA relative transcription level was the highest (0.0721 +/- 0.0187) and it was 0.0089 +/- 0.0037 in control group. CTGF mRNA relative transcription level reached the highest value (0.1136 +/- 0.0365) in 12 weeks after infection, while it was 0.0293 +/- 0.0184 in control group. CTGF mRNA expression was positively correlated with the duration of infection (r = 0.927, NO.05). CONCLUSIONS The area and cell types of TGFb1 positive expression is the same as that of CTGF in liver tissue of schistosome infected mice (BALB/c). CTGF mRNA expression is significantly related to the duration of infection, but it is not the case for TGFbl.

UI MeSH Term Description Entries
D008099 Liver A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances. Livers
D008103 Liver Cirrhosis Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. Cirrhosis, Liver,Fibrosis, Liver,Hepatic Cirrhosis,Liver Fibrosis,Cirrhosis, Hepatic
D008297 Male Males
D008807 Mice, Inbred BALB C An inbred strain of mouse that is widely used in IMMUNOLOGY studies and cancer research. BALB C Mice, Inbred,BALB C Mouse, Inbred,Inbred BALB C Mice,Inbred BALB C Mouse,Mice, BALB C,Mouse, BALB C,Mouse, Inbred BALB C,BALB C Mice,BALB C Mouse
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D012333 RNA, Messenger RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm. Messenger RNA,Messenger RNA, Polyadenylated,Poly(A) Tail,Poly(A)+ RNA,Poly(A)+ mRNA,RNA, Messenger, Polyadenylated,RNA, Polyadenylated,mRNA,mRNA, Non-Polyadenylated,mRNA, Polyadenylated,Non-Polyadenylated mRNA,Poly(A) RNA,Polyadenylated mRNA,Non Polyadenylated mRNA,Polyadenylated Messenger RNA,Polyadenylated RNA,RNA, Polyadenylated Messenger,mRNA, Non Polyadenylated
D012554 Schistosomiasis japonica Schistosomiasis caused by Schistosoma japonicum. It is endemic in the ASIA, EASTERN and affects the bowel, liver, and spleen. Schistosoma japonicum Infection,Schistosomiasis japonicum,Infection, Schistosoma japonicum,Infections, Schistosoma japonicum,Schistosoma japonicum Infections
D051379 Mice The common name for the genus Mus. Mice, House,Mus,Mus musculus,Mice, Laboratory,Mouse,Mouse, House,Mouse, Laboratory,Mouse, Swiss,Mus domesticus,Mus musculus domesticus,Swiss Mice,House Mice,House Mouse,Laboratory Mice,Laboratory Mouse,Mice, Swiss,Swiss Mouse,domesticus, Mus musculus
D053773 Transforming Growth Factor beta1 A subtype of transforming growth factor beta that is synthesized by a wide variety of cells. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta 1 and TGF-beta1 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor. Defects in the gene that encodes TGF-beta1 are the cause of CAMURATI-ENGELMANN SYNDROME. TGF-beta1,Transforming Growth Factor-beta1,TGF-beta-1,TGF-beta1 Latency-Associated Protein,TGF-beta1LAP,Transforming Growth Factor beta 1 Latency Associated Peptide,Transforming Growth Factor beta I,Latency-Associated Protein, TGF-beta1,TGF beta 1,TGF beta1 Latency Associated Protein,TGF beta1LAP

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