Gene and protein expression of protease-activated receptor-1, 2 in a routine model of acute graft-versus-host disease
10.3760/cma.j.issn.0254-1785.2009.07.005
- VernacularTitle:蛋白酶激活受体-1,2在小鼠急性移植物抗宿主病模型中的表达
- Author:
Quan LI
;
Jian ZHANG
;
Ping ZOU
;
Weiming LI
- Publication Type:Journal Article
- Keywords:
Acute graft-versus-host disease;
Protease-aetivated receptor;
Hematopoietic stem cell transplantation
- From:
Chinese Journal of Organ Transplantation
2009;30(7):407-410
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the expression of protease-aetivated receptor (PAR)-1, 2 in a routine model of acute graft-versus-host disease (aGVHD). Methods A routine model of aGVHD after aUogeneic hematopoietic stem cell transplantation (allo-HSCT) was established, and the syngeneic HSCT mice were used as the controls. Quantitative real-time PCR, Western blot and immunohistoehemistry were done to detect the gene and protein expression of PAR-1, 2 in multiple organs of allo-HSCT mice and the controls. Results Allo-HSCT mice showed classical symptoms and histological changes of aGVHD. PAR-1 mRNA expression was significantly increased in the skin,liver, small intestine of allo-HSCT mice (skin: 0. 039 ± 0. 013 vs. controls: 0. 008 ± 0. 002,P<0. 01 liver: 0. 165 ± 0. 084, vs. controls: 0. 017 ± 0. 006, P<0. 01 ; small intestine: 0. 215 ± 0. 109 vs.controls: 0. 016±0. 009, P<0. 01), but not in the stomach, lung and kidney of allo-HSCT mice (P >0. 05). PAR-2 mRNA expression in the liver and small intestine of allo-HSCT mice was significantly elevated (liver: 0. 010 ± 0. 003 vs. controls: 0. 003 ± 0. 002, P<0. 01 ; small intestine:0. 006 ± 0. 002 vs. controls: 0. 003± 0. 002,P<0. 05), but not in the other organs (P>0. 05). The protein expression of PAR-1, 2 was in accordance with the mRNA expression. Immunohistochemistry revealed the PAR-1, 2 expression was increased in the epithelial eeUs and vascular endothelial cells of target organs of aGVHD. Conclusion Inereased expression of PAR-1, 2 in the target organs of aGVHD suggests PAR-1, 2 may contribute to the pathogenesis of aGVHD after allo-HSCT.
