| First Author | Castagliuolo I | Year | 2002 |
| Journal | Br J Pharmacol | Volume | 136 |
| Issue | 2 | Pages | 271-9 |
| PubMed ID | 12010776 | Mgi Jnum | J:103176 |
| Mgi Id | MGI:3608587 | Doi | 10.1038/sj.bjp.0704697 |
| Citation | Castagliuolo I, et al. (2002) Protective effects of neurokinin-1 receptor during colitis in mice: role of the epidermal growth factor receptor. Br J Pharmacol 136(2):271-9 |
| abstractText | 1. The role of substance P and its high affinity neurokinin-1 receptor in colitis has not been fully elucidated. We assessed the participation of neurokinin-1 receptor in colitis using the 2,4,6,-trinitrobenzensulphonic acid and dextran sulphate-induced animal models of colitis and genetically-engineered, neurokinin-1 receptor-deficient mice. 2. Clinical signs, macroscopic and histologic damage associated with 2,4,6,-trinitrobenzensulphonic acid (12 days) and dextran sulphate (5 days) colitis were more severe in neurokinin-1 deficient than in wild-type mice, while immunoreactivities for epidermal growth factor and its receptor were similar in the colon of both mice strains before and after colitis. 3. Substance P, dose-dependently induced intestinal fibroblast proliferation and enhanced epidermal growth factor-induced proliferation in intestinal fibroblasts isolated from wild-type, but not from neurokinin-1 receptor deficient mice. 4. Substance P-induced intestinal fibroblast proliferation required the presence of epidermal growth factor receptor with kinase activity. Furthermore, substance P induced epidermal growth factor tyrosine phosphorylation and activation in normal intestinal fibroblasts. 5. Our results indicate that in mice lacking the neurokinin - 1 receptor, substance P plays a protective role in prolonged experimental colitis. |
