37 research outputs found
Colitis induced by proteinase-activated receptor-2 agonists is mediated by a neurogenic mechanism
Kallikrein-related peptidases (KLKs), Proteinase-mediated Signalling and Proteinase-activated receptors (PARs)
Synthesis and activities of cyclic thrombin-receptor-derived peptide analogues of the Ser42-Phe-Leu-Leu-Arg46 motif sequence containing d-Phe and/or d-Arg
The similarities and dissimilarities of insulin and oxytocin in regulation of glucose metabolism in isolated rat adipocytes
Σύνθεση και βιολογική δράση κυκλικών αναλόγων του επιτόπου της θρομβίνης με την αλληλουχία Ser42-Phe-Leu-Arg46. Η αναγκαιότητα της προσέγγισης των δραστικών ομάδων Phe-Arg αμινομάδας για βιολογική δράση
Mucosal Allergic Sensitization to Cockroach Allergens Is Dependent on Proteinase Activity and Proteinase-Activated Receptor-2 Activation
Supplementary Material for: Cathelicidins Induce Toll-Interacting Protein Synthesis to Prevent Apoptosis in Colonic Epithelium
Cathelicidin peptides secreted by leukocytes and epithelial cells are microbicidal but also regulate pathogen sensing via toll-like receptors (TLRs) in the colon by mechanisms that are not fully understood. Herein, analyses with the attaching/effacing pathogen Citrobacter rodentium model of colitis in cathelicidin-deficient (Camp−/−) mice, and colonic epithelia demonstrate that cathelicidins prevent apoptosis by sustaining post-transcriptional synthesis of a TLR adapter, toll-interacting protein (TOLLIP). Cathelicidins induced phosphorylation-activation of epidermal growth factor receptor (EGFR)-kinase, which phosphorylated-inactivated miRNA-activating enzyme Argonaute 2 (AGO2), thus reducing availability of the TOLLIP repressor miRNA-31. Cathelicidins promoted stability of TOLLIP protein via a proteosome-dependent pathway. This cathelicidin-induced TOLLIP upregulation prevented apoptosis in the colonic epithelium by reducing levels of caspase-3 and poly (ADP-ribose) polymerase (PARP)-1 in response to the proinflammatory cytokines, interferon-γ (IFNγ) and tumor necrosis factor-α (TNFα). Further, Camp−/− colonic epithelial cells were more susceptible to apoptosis during C. rodentium infection than wild-type cells. This antiapoptotic effect of cathelicidins, maintaining epithelial TOLLIP protein in the gut, provides insight into cathelicidin’s ability to regulate TLR signaling and prevent exacerbated inflammation