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Pro- and Anti-Inflammatory Cytokine Signaling within 3D Tissue Models
Published in Karen J.L. Burg, Didier Dréau, Timothy Burg, Engineering 3D Tissue Test Systems, 2017
Stephen L. Rego, Tian McCann, Didier Dréau
Cytokines elicit their effects by binding to their cognate receptors on target cells and activating an array of signaling cascades, including but not limited to those summarized in Figure 12.2. The signaling cascades activated by cytokines are context and cell specific and it is not uncommon for a single cytokine to activate multiple signaling pathways. For example, the canonical inflammatory cytokine, TNF, upon binding to its receptor activates both caspase dependent and independent signaling events (Rath and Aggarwal 1999; Koul et al. 2006). The activated TNFR recruits a number of effector proteins including TNFR-Associated Death Domain protein (TRADD) which in turn recruits Fas-Associated Death Domain (FADD), TNF Receptor-Associated Factor-2 (TRAF2), and Receptor-Interacting Protein (RIP). TRADD and FADD recruitment to the TNFR leads to activation of the caspase cascade and ultimately apoptosis. TRAF2 and RIP lead to activation of the Activation Protein-1 (AP-1) and NFκB pathways that have pleiotropic effects on cellular behaviors (Henkler et al. 2003; Wajant et al. 2003).
Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Margaux Cochard, Frédéric Ledoux, Yann Landkocz
The most involved pathways include the TGF-β superfamily with formation of complex SMAD2/3 and SMAD4 (Kolosova, Nethery, and Kern 2011; Valcourt et al. 2005) and its translocation through the nucleus, activation of TNF receptor-associated factor 6 (TRAF6) followed by stimulation of p38 MAPK and JUN N-terminal kinase (JNK) (Kolosova, Nethery, and Kern 2011; Yamashita et al. 2008), and the phosphatidylinositol 3-kinases (PI3K) through the PI3K/protein kinase B (AKT)/β-catenin pathway (Bakin et al. 2000; Lamouille et al. 2012; Wang et al. 2014). The PI3K/AKT/β-catenin pathway is also linked to Wnt, integrins and tyrosine kinase receptors pathways. In this pathway, activation of AKT inhibits glycogen synthase kinase-3β (GSK-3β) (Bachelder et al. 2005) to stabilize β-catenin. β-catenin is therefore able to translocate in the nucleus to engage lymphoid enhancer-binding factor 1 (LEF) (Nawshad et al. 2007) and T cell factor (TCF) which promote EMT transcription factors (Lamouille, Xu, and Derynck 2014).