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Expression of protease-activated receptor 2 in ulcerative colitis
Jin-A Kim1, Suck-Chei Choi, Ki-Jung Yun
1Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University School of Medicine, Iksan, Chonbuk, South Korea.
Inflammatory Bowel Diseases
|August 7, 2003
Summary
Protease-activated receptor 2 (PAR2) activation in mast cells may drive ulcerative colitis (UC) pathogenesis. This study found increased PAR2 and TNF-alpha in UC tissues, suggesting PAR2
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Mast cells and tryptase are implicated in ulcerative colitis (UC) pathogenesis.
- The role of protease-activated receptor 2 (PAR2), a tryptase receptor, in UC remains unclear.
Purpose of the Study:
- To investigate the expression and role of PAR2 and tumor necrosis factor (TNF)-alpha in UC tissues.
- To determine if PAR2 activation influences TNF-alpha secretion from mast cells.
Main Methods:
- Immunohistochemistry was used to examine PAR2 and TNF-alpha expression in UC and normal tissues.
- Enzyme-linked immunosorbent assay (ELISA) measured TNF-alpha secretion from HMC-1 cells after PAR2 agonist treatment.
Main Results:
- PAR2 and TNF-alpha proteins were significantly elevated in UC tissues compared to normal tissues.
- A significant correlation was observed between PAR2 and TNF-alpha in tryptase-positive mast cells from UC tissues.
- PAR2 agonists significantly induced TNF-alpha secretion from HMC-1 cells.
Conclusions:
- Mast cell activation via PAR2 may contribute to the pathogenesis of ulcerative colitis.
- Targeting the PAR2 pathway could offer a therapeutic strategy for UC.
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