Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3292776 | Gastroenterology | 2015 | 18 Pages |
Abstract
In mice, plasmin induces a feedback mechanism in which activation of the fibrinolytic system promotes the development of colitis via activation of MMP9 or proteolytic enzymes. The proteolytic environment stimulates the influx of myeloid cells into the colonic epithelium and the production of tumor necrosis factor and C-X-C motif chemokine ligand 5. In turn, myeloid CD11b+ cells release the urokinase plasminogen activator, which accelerates plasmin production. Disruption of the plasmin-induced chronic inflammatory circuit therefore might be a strategy for colitis treatment.
Keywords
plasmin-antiplasmin complexTNFDSSIBDFDPPAPDAIMMPPLGCXCL5TNBSTrinitrobenzene sulfonic acidinterleukinInflammatory bowel diseaseDextran sulfate sodiumdisease activity indextumor necrosis factorplasminogen activatorurokinase-type plasminogen activatormatrix metalloproteinasefibrin degradation productMouse modelAntibodyPlasminogen
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Authors
Shinya Munakata, Yoshihiko Tashiro, Chiemi Nishida, Aki Sato, Hiromitsu Komiyama, Hiroshi Shimazu, Douaa Dhahri, Yousef Salama, Salita Eiamboonsert, Kazuyoshi Takeda, Hideo Yagita, Yuko Tsuda, Yoshio Okada, Hiromitsu Nakauchi, Kazuhiro Sakamoto,