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Secreted effectors of the innate mucosal barrier
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Michael A. McGuckin, Andre J. Ouellette, Gary D. Wu
The Wnt pathway regulates cellular differentiation of the intestinal epithelium in several ways. First, the β-catenin/TCF transcriptional complex activates genes expressing Ephrin-B ligands and their receptors EphB, which have a role in establishing migratory pathways as well as maintaining cellular boundaries. The gradient of EphB receptor expression within the crypt maintains the correct cellular architecture with CBCs and Paneth cells located at the base of the crypt compartment. Deletion of EphB3 results in aberrant Paneth cell localization. Second, signaling through the Wnt pathway is required for Paneth cell maturation and their expression of antimicrobial peptides. Furthermore, the Wnt-dependent SOX9 gene is critical for Paneth cell development, because mice with a conditional deletion of Sox9 lack Paneth cells completely. Finally, Wnt signaling may have an effect on cell fate determination by impeding terminal differentiation of secretory cell lineages. TCF4−/− mice have goblet cells and enterocytes but lack enteroendocrine cells, whereas transgenic overexpression of Dkk1, an inhibitor of Wnt signaling, ablates the secretory cell lineages while absorptive enterocytes remain normal.
Endothelium
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
The maturation of new endothelial tubes into arterioles and venules is brought about by the recruitment of smooth muscle cells and connective tissue cells, driven by platelet-derived growth factor (PDGF) and angiopoietins. The final fate of the vessel, that is, whether it becomes an artery or vein, is determined by the expression of the protein ephrin-B and its receptor.
Osteoimmunology in Aging
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Lia Ginaldi, Daniela Di Silvestre, Maria Maddalena Sirufo, Massimo De Martinis
Many other receptor pathways, most of which are shared by immune cells, interact with RANK, some co-stimulators and others inhibitors. The inhibitor receptor system ephrin (Eph) B2/B4 allows the passage of signals bidirectionally between osteoclasts and osteoblasts [54]. It inhibits osteoclast differentiation by blocking c-fos and the NFATc1 transcriptional cascade in osteoclast cell lineage and contemporaneously favors the coupling of bone formation and resorption through the induction of osteogenetic regulatory genes in osteoblasts [55]. The ephrinB2/ephrinB4 binding therefore functions as a coupling factor in bone remodeling process [56]. Other coupling factors are semaphorins, glycoproteins involved in several biological processes such as immune response, tumor progression, and bone remodeling, among others [57–59]. Semaphorin4D (Sema4D) expressed in osteoclasts binds to its osteoblast receptor (Plexin-B1) inhibiting IGF-1 pathway, essential for osteoblast differentiation [60], whereas Sema3A in osteoblasts is an inhibitor of osteoclastogenesis [61]. During bone remodeling osteoclasts inhibit bone formation by expressing Sema4D, in order to initiate bone resorption, whereas osteoblasts express Sema3A that suppresses bone resorption, prior to bone formation.
Proteomic approaches to assist in diagnosis and prognosis of oral cancer
Published in Expert Review of Proteomics, 2021
Jamile De Oliveira Sá, Luciana Daniele Trino, Ana Karina Oliveira, Ariane Fidelis Busso Lopes, Daniela Campos Granato, Ana Gabriela Costa Normando, Erison Santana Santos, Leandro Xavier Neves, Carolina Moretto Carnielli, Adriana Franco Paes Leme
EVs isolated from the PE/CA-PJ49/E10 OSCC cell line were shown to highly express proteins involved in angiogenesis, proliferation, migration, and adhesion, especially EGFR and ITGB4 [69]. The proteome associated with angiogenesis was prioritized in EVs from 3 HNSCC cells, including two oral cancer cell lines – SCC61 and OSC19, and a pharynx cell line – Detroit 562 [70]. Label-free MS revealed 1,016 and 1,237 unique proteins in OSC19 and Detroit 562-EVs, respectively. The proteome from SCC61-derived EVs was retrieved from the literature [71]. Several ephrins and ephrin receptors (Eph) family proteins were detected in vesicles from the three cells, and analysis revealed EPHB2 as a promising candidate to have a role in EV-mediated angiogenesis. Further experiments confirmed that EPHB2 expression in HNSCC cells promotes tumor angiogenesis in an orthotopic mouse model and suggest that EPHB2 may recruit blood vessels into tumors, facilitating tumor survival and promoting metastasis.
The role of Eph receptors in cancer and how to target them: novel approaches in cancer treatment
Published in Expert Opinion on Investigational Drugs, 2020
Oscar J Buckens, Btissame El Hassouni, Elisa Giovannetti, Godefridus J Peters
The difference between Ephrin A and Ephrin B ligands is the binding of the ligand to the cell surface bound receptor. Ephrin A ligands are attached to the membrane through a glycophosphatidylinositol anchor, while Ephrin B ligands possess a trans-membrane region consisting of a PDZ domain and a cytoplasmic region [2,6]. The PDZ binding motif of Ephrin B plays an important role in the bi-directional signaling of the Eph/Ephrin system [6]. Besides, the receptors differ in the way the ligands bind to the receptors. EphA receptors barely need to undergo any conformational changes to bind to their ligands, while EphB receptors have to slightly rearrange their ligand-binding site [10]. Nevertheless, both receptors have the ability to form strong structures with their respective ligands, making it possible to let drugs intervene with these interactions [4]. Another region for drug targeting is the kinase domain of the receptors [13,14]. In general, Ephrin B ligands bind to EphB receptors and EphrinA ligands bind to EphA receptors, with the exception of EphA4, which also binds to EphrinB2, and EphB2, which also binds to EphrinA5 [3].
Lithium-induced gene expression alterations in two peripheral cell models of bipolar disorder
Published in The World Journal of Biological Psychiatry, 2019
Sarah Kittel-Schneider, Max Hilscher, Claus-Jürgen Scholz, Heike Weber, Lena Grünewald, Ricarda Schwarz, Andreas G. Chiocchetti, Andreas Reif
EPHB1 codes for a protein called Ephrin type B receptor 1. Ephrin receptors and their ligands, the ephrins, play a role in numerous developmental processes, also in the central nervous system. Ephrin receptors are part of the receptor tyrosine kinase family (Flanagan and Vanderhaeghen 1998). Furthermore, they seem to play a role in inflammatory and neuropathic pain (Cibert-Goton et al. 2013). Most interestingly, in our study, lithium treatment showed to have opposing effects in cells of bipolar patients and controls. EPHB1 expression was upregulated in control cells and downregulated in bipolar cells due to lithium treatment. In the GWAS data sets, a single-nucleotide polymorphism of EPBH1 gene (rs66745619) has been shown to be associated with BD and other single-nucleotide polymorphisms in EPHB1 (rs7635276, rs7613488 and rs35879719) were associated with lithium response in the ConLiGen GWAS dataset. To clarify the underlying molecular processes, further studies are needed.