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Journal articles on the topic 'EphrineB2'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Liu, Hui, Kavi Devraj, Kerstin Möller, Stefan Liebner, Markus Hecker, and Thomas Korff. "EphrinB-mediated reverse signalling controls junctional integrity and pro-inflammatory differentiation of endothelial cells." Thrombosis and Haemostasis 112, no. 07 (2014): 151–63. http://dx.doi.org/10.1160/th13-12-1034.

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SummaryThe EphB/ephrinB receptor-ligand system is pivotal for the development of the embryonic vasculature and for angiogenesis in the adult organism. We observed that (i) the expression of ephrinB2 and ephrinB1 is up-regulated in capillaries during inflammation, that (ii) these ligands are localised on the luminal endothelial surface, and that (iii) they interact with the ephrinB-receptor EphB2 on monocyte/macrophages. This study delineates the impact of ephrinB-mediated reverse signalling on the integrity and proinflammatory differentiation of the endothelium. To this end, in vitro analyses

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2

Negrete, Oscar A., David Chu, Hector C. Aguilar, and Benhur Lee. "Single Amino Acid Changes in the Nipah and Hendra Virus Attachment Glycoproteins Distinguish EphrinB2 from EphrinB3 Usage." Journal of Virology 81, no. 19 (2007): 10804–14. http://dx.doi.org/10.1128/jvi.00999-07.

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ABSTRACT The henipaviruses, Nipah virus (NiV) and Hendra virus (HeV), are lethal emerging paramyxoviruses. EphrinB2 and ephrinB3 have been identified as receptors for henipavirus entry. NiV and HeV share similar cellular tropisms and likely use an identical receptor set, although a quantitative comparison of receptor usage by NiV and HeV has not been reported. Here we show that (i) soluble NiV attachment protein G (sNiV-G) bound to cell surface-expressed ephrinB3 with a 30-fold higher affinity than that of sHeV-G, (ii) NiV envelope pseudotyped reporter virus (NiVpp) entered ephrinB3-expressing

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PRESTOZ, LAETITIA, ELLI CHATZOPOULOU, GREGORY LEMKINE, et al. "Control of axonophilic migration of oligodendrocyte precursor cells by Eph–ephrin interaction." Neuron Glia Biology 1, no. 1 (2004): 73–83. http://dx.doi.org/10.1017/s1740925x04000109.

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The migration of oligodendrocyte precursor cells (OPCs) is modulated by secreted molecules in their environment and by cell–cell and matrix–cell interactions. Here, we ask whether membrane-anchored guidance cues, such as the ephrin ligands and their Eph receptors, participate in the control of OPC migration in the optic nerve. We postulate that EphA and EphB receptors, which are expressed on axons of retinal ganglion cells, interact with ephrins on the surface of OPCs. We show the expression of ephrinA5, ephrinB 2 and ephrinB3 in the migrating OPCs of the optic nerve as well as in the dienceph

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Yan, Min. "EphrinB-EphB Signaling Induces Hyperalgesia through ERK5/CREB Pathway in Rats." May 2017 4, no. 20;4 (2017): E563—E574. http://dx.doi.org/10.36076/ppj.2017.e574.

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Background: There are numerous studies implicating that EphB receptors and ephrinB ligands play important roles in modulating the transduction of spinal nociceptive information. EphrinB-EphB signaling may contribute to hyperalgesia via various kinds of downstream molecules, the mechanisms of which have not been completely understood. Objective: The aim of the present study was to identify whether ephrinB-EphB signaling could contribute to hyperalgesia through ERK5/CREB pathway. Study Design: Controlled animal study. Setting: University laboratory. Methods: This study attempted to detect the ch

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Kitamura, Takuya, Yukihito Kabuyama, Akihisa Kamataki, et al. "Enhancement of lymphocyte migration and cytokine production by ephrinB1 system in rheumatoid arthritis." American Journal of Physiology-Cell Physiology 294, no. 1 (2008): C189—C196. http://dx.doi.org/10.1152/ajpcell.00314.2007.

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Although the etiology of early events in rheumatoid arthritis (RA) remains undefined, an anomaly in T cell homeostasis and hyperproliferation of synovial-lining cells are involved in the disease process. Since it has been reported that the ephrin/Eph receptor system plays important signaling roles in inflammation processes, we attempted to examine ephrinB molecules in T cells and synovial cells derived from RA in this study. The expression level of ephrinB1 was significantly high in synovial fibroblasts and CD3-positive exudate lymphocytes in synovial tissues derived from patients with RA comp

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BONG, Yong-Sik, Yeon-Hwa PARK, Hyun-Shik LEE, Kathleen MOOD, Akihiko ISHIMURA, and Ira O. DAAR. "Tyr-298 in ephrinB1 is critical for an interaction with the Grb4 adaptor protein." Biochemical Journal 377, no. 2 (2004): 499–507. http://dx.doi.org/10.1042/bj20031449.

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The Eph family of receptor tyrosine kinases and their membrane-bound ligands, the ephrins, are thought to play a role in the regulation of cell adhesion and migration during development by mediating cell-to-cell signalling events. The transmembrane ephrinB protein is a bidirectional signalling molecule that sends a forward signal through the activation of its cognate receptor tyrosine kinase residing on another cell. The reverse signal is transduced into the ephrinB-expressing cell via tyrosine phosphorylation of its conserved C-terminal cytoplasmic domain. Previous work from our laboratory ha

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7

Bishop, Kimberly A., Tzanko S. Stantchev, Andrew C. Hickey, et al. "Identification of Hendra Virus G Glycoprotein Residues That Are Critical for Receptor Binding." Journal of Virology 81, no. 11 (2007): 5893–901. http://dx.doi.org/10.1128/jvi.02022-06.

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ABSTRACT Hendra virus (HeV) is an emerging paramyxovirus capable of infecting and causing disease in a variety of mammalian species, including humans. The virus infects its host cells through the coordinated functions of its fusion (F) and attachment (G) glycoproteins, the latter of which is responsible for binding the virus receptors ephrinB2 and ephrinB3. In order to identify the receptor binding site, a panel of G glycoprotein constructs containing mutations was generated using an alanine-scanning mutagenesis strategy. Based on a predicted G structure, charged amino acids residing in region

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8

Lee, Benhur, Olivier Pernet, Asim A. Ahmed, Antra Zeltina, Shannon M. Beaty, and Thomas A. Bowden. "Molecular recognition of human ephrinB2 cell surface receptor by an emergent African henipavirus." Proceedings of the National Academy of Sciences 112, no. 17 (2015): E2156—E2165. http://dx.doi.org/10.1073/pnas.1501690112.

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The discovery of African henipaviruses (HNVs) related to pathogenic Hendra virus (HeV) and Nipah virus (NiV) from Southeast Asia and Australia presents an open-ended health risk. Cell receptor use by emerging African HNVs at the stage of host-cell entry is a key parameter when considering the potential for spillover and infection of human populations. The attachment glycoprotein from a Ghanaian bat isolate (GhV-G) exhibits <30% sequence identity with Asiatic NiV-G/HeV-G. Here, through functional and structural analysis of GhV-G, we show how this African HNV targets the same human cell-surfa

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Ruan, Jia-Ping, Hong-Xing Zhang, Xian-Fu Lu, Yue-Peng Liu, and Jun-Li Cao. "EphrinBs/EphBs Signaling Is Involved in Modulation of Spinal Nociceptive Processing through a Mitogen-activated Protein Kinases-dependent Mechanism." Anesthesiology 112, no. 5 (2010): 1234–49. http://dx.doi.org/10.1097/aln.0b013e3181d3e0df.

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Background Our previous studies have demonstrated that EphBs receptors and ephrinBs ligands were involved in modulation of spinal nociceptive information. However, the downstream mechanisms that control this process are not well understood. The aim of this study was to further investigate whether mitogen-activated protein kinases (MAPKs), as the downstream effectors, participate in modulation of spinal nociceptive information related to ephrinBs/EphBs. Methods Thermal hyperalgesia and mechanical allodynia were measured using radiant heat and von Frey filaments test. Immunofluorescence staining

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Wu, Hsi-Chin, Chao-Hsiang Chang, Hsien-Yu Peng, et al. "EphrinB2 induces pelvic-urethra reflex potentiation via Src kinase-dependent tyrosine phosphorylation of NR2B." American Journal of Physiology-Renal Physiology 300, no. 2 (2011): F403—F411. http://dx.doi.org/10.1152/ajprenal.00520.2010.

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Recently, the role of EphB receptor (EphBR) tyrosine kinase and their ephrinB ligands in pain-related neural plasticity at the spinal cord level have been identified. To test whether Src-family tyrosine kinase-dependent glutamatergic N-methyl-d-aspartate receptor NR2B subunit phosphorylation underlies lumbosacral spinal EphBR activation to mediate pelvic-urethra reflex potentiation, we recorded external urethra sphincter electromyogram reflex activity and analyzed protein expression in the lumbosacral (L6-S2) dorsal horn in response to intrathecal ephrinB2 injections. When compared with vehicl

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Riedl, Jurgen A., Dominique T. Brandt, Eduard Batlle, Leo S. Price, Hans Clevers, and Johannes L. Bos. "Down-regulation of Rap1 activity is involved in ephrinB1-induced cell contraction." Biochemical Journal 389, no. 2 (2005): 465–69. http://dx.doi.org/10.1042/bj20050048.

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Ephrins are cell surface ligands that activate Eph receptor tyrosine kinases. This ligand–receptor interaction plays a central role in the sorting of cells. We have previously shown that the ephrinB–EphB signalling pathway is also involved in the migration of intestinal precursor cells along the crypts. Using the colon cell line DLD1 expressing the EphB2 receptor, we showed that stimulation of these cells with soluble ephrinB1 results in a rapid retraction of cell extensions and a detachment of cells. On ephrinB1 stimulation, the small GTPases Rho and Ras are activated and Rap1 is inactivated.

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12

Aguilar, Hector C., Vanessa Aspericueta, Lindsey R. Robinson, Karen E. Aanensen, and Benhur Lee. "A Quantitative and Kinetic Fusion Protein-Triggering Assay Can Discern Distinct Steps in the Nipah Virus Membrane Fusion Cascade." Journal of Virology 84, no. 16 (2010): 8033–41. http://dx.doi.org/10.1128/jvi.00469-10.

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ABSTRACT The deadly paramyxovirus Nipah virus (NiV) contains a fusion glycoprotein (F) with canonical structural and functional features common to its class. Receptor binding to the NiV attachment glycoprotein (G) triggers F to undergo a two-phase conformational cascade: the first phase progresses from a metastable prefusion state to a prehairpin intermediate (PHI), while the second phase is marked by transition from the PHI to the six-helix-bundle hairpin. The PHI can be captured with peptides that mimic F's heptad repeat regions, and here we utilized a NiV heptad repeat peptide to quantify P

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Zhou, Xuan, Liu Xiaoli, Na Xu, et al. "EphrinB2/EphB4 Interaction Promotes Myeloid Leukemia Cell Invasion through RhoA-Mediated Mechanism." Blood 124, no. 21 (2014): 1018. http://dx.doi.org/10.1182/blood.v124.21.1018.1018.

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Abstract Background and Objective: Several studies have reported the up-regulation of EphB receptor-tyrosine kinases and ephrinB ligands in a variety of tumors, suggesting a functional relation between EphB/ephrinB signaling and tumor progression. However, how they regulate the invasiveness of myeloid leukemia cells were still unknown. Our previously study suggested that EphB4 were highly expressed in patients with extramedullary leukemia compared with patients without extramedullary leukemia, which indicated that the expression of EphB4 was related with myeloid leukemia cell invasion. To addr

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Kumar, R. Sreeraman, R. J. B. Macaulay, H. C. Rutherford, N. Barkey, J. Koomen, and D. L. Morse. "EphrinB3 and EphrinB4 Receptors are potential therapeutic targets in glioblastoma." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S3 (2015): S4. http://dx.doi.org/10.1017/cjn.2015.373.

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15

Peng, Hsien-Yu, Gin-Den Chen, Cheng-Hung Lai, Kwong-Chung Tung, Junn-Liang Chang, and Tzer-Bin Lin. "Endogenous ephrinB2 mediates colon-urethra cross-organ sensitization via Src kinase-dependent tyrosine phosphorylation of NR2B." American Journal of Physiology-Renal Physiology 298, no. 1 (2010): F109—F117. http://dx.doi.org/10.1152/ajprenal.00287.2009.

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Recently, the role of EphB receptor (EphBR) tyrosine kinase and their ephrinB ligands in spinal pain-related neural plasticity has been identified. To test whether Src-family non-receptor tyrosine kinase-dependent glutamatergic N-methyl-d-aspartate receptor (NMDAR) NR2B subunit phosphorylation underlies lumbosacral spinal EphBR activation to mediate cross-organ sensitization between the colon and the urethra, external urethra sphincter electromyogram activity evoked by pelvic nerve stimulation and protein expression in the lumbosacral (L6–S2) dorsal horn were studied before and after intracolo

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16

Luo, Hongyu, Bieke Broux, Xuehai Wang, et al. "EphrinB1 and EphrinB2 regulate T cell chemotaxis and migration in experimental autoimmune encephalomyelitis and multiple sclerosis." Neurobiology of Disease 91 (July 2016): 292–306. http://dx.doi.org/10.1016/j.nbd.2016.03.013.

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17

Gerety, Sebastian S., and David J. Anderson. "Cardiovascular ephrinB2 function is essential for embryonic angiogenesis." Development 129, no. 6 (2002): 1397–410. http://dx.doi.org/10.1242/dev.129.6.1397.

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EphrinB2, a transmembrane ligand of EphB receptor tyrosine kinases, is specifically expressed in arteries. In ephrinB2 mutant embryos, there is a complete arrest of angiogenesis. However, ephrinB2 expression is not restricted to vascular endothelial cells, and it has been proposed that its essential function may be exerted in adjacent mesenchymal cells. We have generated mice in which ephrinB2 is specifically deleted in the endothelium and endocardium of the developing vasculature and heart. We find that such a vascular-specific deletion of ephrinB2 results in angiogenic remodeling defects ide

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18

Fehnel, Katie Pricola, David L. Penn, Micah Duggins-Warf, et al. "Dysregulation of the EphrinB2−EphB4 ratio in pediatric cerebral arteriovenous malformations is associated with endothelial cell dysfunction in vitro and functions as a novel noninvasive biomarker in patients." Experimental & Molecular Medicine 52, no. 4 (2020): 658–71. http://dx.doi.org/10.1038/s12276-020-0414-0.

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Abstract We investigated (1) EphrinB2 and EphB4 receptor expression in cerebral AVMs, (2) the impact of an altered EphrinB2:EphB4 ratio on brain endothelial cell function and (3) potential translational applications of these data. The following parameters were compared between AVM endothelial cells (AVMECs) and human brain microvascular endothelial cells (HBMVECs): quantified EphrinB2 and EphB4 expression, angiogenic potential, and responses to manipulation of the EphrinB2:EphB4 ratio via pharmacologic stimulation/inhibition. To investigate the clinical relevance of these in vitro data, Ephrin

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Xing, Shihui, Nannan Pan, Wei Xu та ін. "EphrinB2 activation enhances angiogenesis, reduces amyloid-β deposits and secondary damage in thalamus at the early stage after cortical infarction in hypertensive rats". Journal of Cerebral Blood Flow & Metabolism 39, № 9 (2018): 1776–89. http://dx.doi.org/10.1177/0271678x18769188.

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Cerebral infarction causes secondary neurodegeneration and angiogenesis in thalamus, which impacts functional recovery after stroke. Here, we hypothesize that activation of ephrinB2 could stimulate angiogenesis and restore the secondary neurodegeneration in thalamus after cerebral infarction. Focal cerebral infarction was induced by middle cerebral artery occlusion (MCAO). Secondary damage, angiogenesis, amyloid-β (Aβ) deposits, levels of ephrinB2 and receptor for advanced glycation end product (RAGE) in the ipsilateral thalamus were determined by immunofluorescence and immunoblot. The contrib

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Zhu, Min, Yu Hua, Jian Tang, Xiaoke Zhao, Ling Zhang, and Yue Zhang. "Lentiviral-mediated ephrin B2 gene modification of rat bone marrow mesenchymal stem cells." Journal of International Medical Research 47, no. 7 (2019): 3282–98. http://dx.doi.org/10.1177/0300060519843023.

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Objective To determine the effect of the upregulation or knockdown of the ephrinB2 ( Efnb2) gene and the effect of EphB4/EphrinB2 signalling in rat bone marrow mesenchymal stem cells (BMSCs). Methods Rat BMSCs were infected with lentivirus vectors carrying EphrinB2 and shRNA-EphrinB2. EphrinB2 mRNA and protein levels were quantified. At 28 days of culture with neuronal cell-conditioned differentiation medium, levels of microtubule-associated protein 2 (MAP2), CD133 and nestin were detected in EphrinB2/BMSCs and shEphrinB2/BMSCs using quantitative polymerase chain reaction and immunofluorescenc

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Wang, Penglai, Wen Wang, Tengyu Geng, et al. "EphrinB2 regulates osteogenic differentiation of periodontal ligament stem cells and alveolar bone defect regeneration in beagles." Journal of Tissue Engineering 10 (January 2019): 204173141989436. http://dx.doi.org/10.1177/2041731419894361.

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EphrinB2, a membrane protein regulating bone homeostasis, has been demonstrated to induce osteogenic gene expression in periodontal ligament fibroblasts. The aim of this study was to explore the effects of ephrinB2 on osteogenic differentiation of periodontal ligament stem cells and on alveolar bone regeneration in vivo. We assessed the osteogenic gene expression and osteogenic differentiation potential of ephrinB2-modified human and canine periodontal ligament stem cells, in which ephrinB2 expression was upregulated via lentiviral vector transduction. EphrinB2-modified canine periodontal liga

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Korff, Thomas, Jennifer Braun, Dennis Pfaff, Hellmut G. Augustin, and Markus Hecker. "Role of ephrinB2 expression in endothelial cells during arteriogenesis: impact on smooth muscle cell migration and monocyte recruitment." Blood 112, no. 1 (2008): 73–81. http://dx.doi.org/10.1182/blood-2007-12-128835.

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Abstract Expression of the arterial marker molecule ephrinB2 in endothelial cells is a prerequisite for adequate remodeling processes of the developing or angiogenic vasculature. Although its role in these processes has been extensively studied, the impact of ephrinB2 on the remodeling of adult arteries is largely unknown. To this end, we analyzed its expression during a biomechanically induced arteriolar remodeling process known as arteriogenesis and noted a significant increase in ephrinB2 expression under these conditions. By examining those biomechanical forces presumed to drive arteriogen

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Pennisi, Angela, Wen Ling, Xin Li, et al. "The ephrinB2/EphB4 axis is dysregulated in osteoprogenitors from myeloma patients and its activation affects myeloma bone disease and tumor growth." Blood 114, no. 9 (2009): 1803–12. http://dx.doi.org/10.1182/blood-2009-01-201954.

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Myeloma bone disease is caused by uncoupling of osteoclastic bone resorption and osteoblastic bone formation. Bidirectional signaling between the cell-surface ligand ephrinB2 and its receptor, EphB4, is involved in the coupling of osteoblastogenesis and osteoclastogenesis and in angiogenesis. EphrinB2 and EphB4 expression in mesenchymal stem cells (MSCs) from myeloma patients and in bone cells in myelomatous bones was lower than in healthy counterparts. Wnt3a induced up-regulation of EphB4 in patient MSCs. Myeloma cells reduced expression of these genes in MSCs, whereas in vivo myeloma cell-co

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Lin, Li, Xu Na, Jiang Zhiwu, et al. "EphB4/ephrinB2 ephrinB1 Interaction Mediated Chronic Myelogenous Leukemia Mesenchymal Stromal Cells Osteogenic Differentiation in Vitro and In Vivo." Blood 128, no. 22 (2016): 1901. http://dx.doi.org/10.1182/blood.v128.22.1901.1901.

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Abstract Background and Objective: Osteoblasts, important of stromal cells in bone marrow microenvironment, maintain HSCs in resting state and protect its' functions. Osteoblasts derived from mesenchymal stem cells (MSCs), which can be differentiated into osteoblast in bone marrow under the regulation of cytokines. Recent studies have indicated that EphB4/ephrinB2 protein participates in the regulation of osteogenesis differentiation of MSCs in bone marrow microenvironment. Our previous study found that EphB4 receptor was over expressed in CML patients and cell lines, which played an important

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Luo, Hongyu, Zenghui Wu, Shijie Qi, Wei Jin, Bing Han та Jiangping Wu. "Ephrinb1 and Ephrinb2 Are Associated with Interleukin-7 Receptor α and Retard Its Internalization from the Cell Surface". Journal of Biological Chemistry 286, № 52 (2011): 44976–87. http://dx.doi.org/10.1074/jbc.m111.316414.

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Abéngozar, María Angeles, Sergio de Frutos, Sergio Ferreiro, et al. "Blocking ephrinB2 with highly specific antibodies inhibits angiogenesis, lymphangiogenesis, and tumor growth." Blood 119, no. 19 (2012): 4565–76. http://dx.doi.org/10.1182/blood-2011-09-380006.

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Abstract Membrane-anchored ephrinB2 and its receptor EphB4 are involved in the formation of blood and lymphatic vessels in normal and pathologic conditions. Eph/ephrin activation requires cell-cell interactions and leads to bidirectional signaling pathways in both ligand- and receptor-expressing cells. To investigate the functional consequences of blocking ephrinB2 activity, 2 highly specific human single-chain Fv (scFv) Ab fragments against ephrinB2 were generated and characterized. Both Ab fragments suppressed endothelial cell migration and tube formation in vitro in response to VEGF and pro

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Yamanda, Shinsuke, Satoru Ebihara, Masanori Asada, et al. "Role of ephrinB2 in nonproductive angiogenesis induced by Delta-like 4 blockade." Blood 113, no. 15 (2009): 3631–39. http://dx.doi.org/10.1182/blood-2008-07-170381.

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Abstract Delta-like 4 (DLL4) is one of the Notch ligands and plays an important role in vascular development. DLL4 blockade inhibits tumor growth by promoting nonproductive angiogenesis, which is characterized by an increase in vascular density and decrease in tissue perfusion. However, a detailed mechanism remains unclear. In this study, newly developed neutralizing antibodies against mouse and human DLL4 were used to investigate the possible involvement of VEGF-DLL4-ephrinB2 cascade in nonproductive angiogenesis caused by DLL4 blockade. DLL4 blockade and soluble ephrinB2 treatment suppressed

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Das, Amitava, Uday Shergill, Lokendra Thakur, et al. "Ephrin B2/EphB4 pathway in hepatic stellate cells stimulates Erk-dependent VEGF production and sinusoidal endothelial cell recruitment." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 6 (2010): G908—G915. http://dx.doi.org/10.1152/ajpgi.00510.2009.

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Chemotaxis signals between hepatic stellate cells (HSC) and sinusoidal endothelial cells (SEC) maintain hepatic vascular homeostasis and integrity and also regulate changes in sinusoidal structure in response to liver injury. Our prior studies have demonstrated that the bidirectional chemotactic signaling molecules EphrinB2 and EphB4 are expressed in HSC. The aim of our present study was to explore whether and how the EphrinB2/EphB4 system in HSC could promote SEC recruitment, which is essential for sinusoidal structure and remodeling. Stimulation of human HSC (hHSC) with chimeric agonists (2

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Su, Sheng-an, Du Yang, Yue Wu та ін. "EphrinB2 Regulates Cardiac Fibrosis Through Modulating the Interaction of Stat3 and TGF-β/Smad3 Signaling". Circulation Research 121, № 6 (2017): 617–27. http://dx.doi.org/10.1161/circresaha.117.311045.

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Rationale: Cardiac fibrosis is a common feature in left ventricular remodeling that leads to heart failure, regardless of the cause. EphrinB2 (erythropoietin-producing hepatoma interactor B2), a pivotal bidirectional signaling molecule ubiquitously expressed in mammals, is crucial in angiogenesis during development and disease progression. Recently, EphrinB2 was reported to protect kidneys from injury-induced fibrogenesis. However, its role in cardiac fibrosis remains to be clarified. Objective: We sought to determine the role of EphrinB2 in cardiac fibrosis and the underlying mechanisms durin

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Ge, Yu-Wei, Kai Feng, Xiao-Liang Liu, et al. "The Recombinant Protein EphB4-Fc Changes the Ti Particle-Mediated Imbalance of OPG/RANKL via EphrinB2/EphB4 Signaling Pathway and Inhibits the Release of Proinflammatory Factors In Vivo." Oxidative Medicine and Cellular Longevity 2020 (June 6, 2020): 1–15. http://dx.doi.org/10.1155/2020/1404915.

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Aseptic loosening caused by wear particles is one of the common complications after total hip arthroplasty. We investigated the effect of the recombinant protein ephB4-Fc (erythropoietin-producing human hepatocellular receptor 4) on wear particle-mediated inflammatory response. In vitro, ephrinB2 expression was analyzed using siRNA-NFATc1 (nuclear factor of activated T-cells 1) and siRNA-c-Fos. Additionally, we used Tartrate-resistant acid phosphatase (TRAP) staining, bone pit resorption, Enzyme-linked immunosorbent assay (ELISA), as well as ephrinB2 overexpression and knockdown experiments to

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Pennisi, Angela, Wen Ling, Xin Li, Jianmei Chen, Sharmin Khan, and Shmuel Yaccoby. "The EphrinB2/EphB4 Axis Is Dysregulated in Osteoprogenitors from Myeloma Patients and Its Activation by EphrinB2-Fc or EhpB4-Fc Affects Myeloma Bone Disease and Tumor Growth in Vivo." Blood 112, no. 11 (2008): 844. http://dx.doi.org/10.1182/blood.v112.11.844.844.

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Abstract Induction of osteolytic bone lesions in myeloma (MM) is caused by an uncoupling of osteoclastic bone resorption and osteoblastic bone formation. Recent studies indicate that in addition to role in cell adhesion, repulsion and neovascularization, bidirectional signaling between the cell surface molecules EphrinB2 and EphB4 also mediates the coupling between osteoblasts and osteoblasts. While mesenchymal stem cells (MSCs) and osteoblasts express the ligand EphrinB2 land its receptor, EphB4, osteoclasts and their precursors mainly express EphrinB2. Forward signaling in MSCs promotes oste

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Gong, T., J. Xu, B. Heng, et al. "EphrinB2/EphB4 Signaling Regulates DPSCs to Induce Sprouting Angiogenesis of Endothelial Cells." Journal of Dental Research 98, no. 7 (2019): 803–12. http://dx.doi.org/10.1177/0022034519843886.

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Dental pulp stem cells (DPSCs) are capable of facilitating angiogenesis resembling pericytes when located adjacent to endothelial cells (ECs). Nevertheless, the precise mechanisms orchestrating their proangiogenic functions remain unclear. Using a 3-dimensional (3-D) fibrin gel model, we aimed to investigate whether EphrinB2/EphB4 signaling in DPSCs plays a role in supporting vascular morphogenesis mediated by ECs, together with the underlying mechanism involved. The EphrinB2/EphB4 signaling was inhibited either by a pharmacological inhibitor of EphB4 receptor or by knocking down the expressio

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Cohen, Kenneth Stuart, Mina Jamali, and Elizabeth Hyjek. "Identification of ephrinB2 positive vessels in non-Hodgkin lymphoma subtypes." Journal of Clinical Oncology 31, no. 15_suppl (2013): e19542-e19542. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e19542.

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e19542 Background: Current anti-angiogenic therapies for tumors target signaling pathways such as VEGF. However, the role of alternative vascular pathways in tumor biology in general, and lymphoma biology specifically, are less well understood. Recently, the Eph receptor tyrosine kinase signaling pathway has emerged as a novel target for therapeutic inhibition. The EphB family member EphB4, and its reverse signaling ligand ephrinB2, are indispensible for developmental angiogenesis. Inhibition of ephrinB2 signaling results in impaired tumor growth in pre-clinical models. We therefore sought to

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Su, Kaiyue, Ningning Lin, Shouqiang Xie, et al. "DNMT3A inhibits E2F1-induced arterial marker expression and impairs angiogenesis in human umbilical artery endothelial cells." Acta Biochimica et Biophysica Sinica 52, no. 11 (2020): 1236–46. http://dx.doi.org/10.1093/abbs/gmaa109.

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Abstract Arterial marker genes EphrinB2 and HEY2 are essential for cardiovascular development and postnatal neovascularization. Our previous study confirmed that E2F1 could activate the transcription of EphrinB2 and HEY2 in human mesenchymal stem cells; however, the detailed mechanism has not been resolved yet. In this study, we focused on the interaction between E2F1 and DNMT3A, a de novo DNA methyltransferase, on regulating the expression of EphrinB2 and HEY2, and explored the potential mechanisms. Gain- and loss-of-function experiments implicated the positive effect of E2F1 on the expressio

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Yuan, Kuo, Tse-Ming Hong, Jeremy J. W. Chen, Wan Hua Tsai, and Ming T. Lin. "Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis." Blood 104, no. 4 (2004): 1025–33. http://dx.doi.org/10.1182/blood-2003-09-3334.

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AbstractEphrinB2 and EphB4, its cognate receptor, are important in the vascular development of the mouse embryo. Their roles in human inflammatory angiogenesis, however, are not well understood. By examining hyperinflammatory lesions, we saw that ephrinB2 was predominantly expressed in macrophage-like cells and EphB4 in small venules. Because macrophages usually transmigrate through postcapillary venules during inflammation, we wanted to explore the downstream effects of EphB4 after binding to ephrinB2. By using cDNA microarray technique and following reverse transcriptase–polymerase chain rea

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Groeger, Gillian, and Catherine D. Nobes. "Co-operative Cdc42 and Rho signalling mediates ephrinB-triggered endothelial cell retraction." Biochemical Journal 404, no. 1 (2007): 23–29. http://dx.doi.org/10.1042/bj20070146.

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Cell repulsion responses to Eph receptor activation are linked to rapid actin cytoskeletal reorganizations, which in turn are partially mediated by Rho–ROCK (Rho kinase) signalling, driving actomyosin contractility. In the present study, we show that Rho alone is not sufficient for this repulsion response. Rather, Cdc42 (cell division cycle 42) and its effector MRCK (myotonic dystrophy kinase-related Cdc42-binding kinase) are also critical for ephrinB-induced cell retraction. Stimulation of endothelial cells with ephrinB2 triggers rapid, but transient, cell retraction. We show that, although m

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Prospéri, Marie-Thérèse, Priscilla Lépine, Florent Dingli, et al. "Myosin 1b functions as an effector of EphB signaling to control cell repulsion." Journal of Cell Biology 210, no. 2 (2015): 347–61. http://dx.doi.org/10.1083/jcb.201501018.

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Eph receptors and their membrane-tethered ligands, the ephrins, have important functions in embryo morphogenesis and in adult tissue homeostasis. Eph/ephrin signaling is essential for cell segregation and cell repulsion. This process is accompanied by morphological changes and actin remodeling that drives cell segregation and tissue patterning. The actin cortex must be mechanically coupled to the plasma membrane to orchestrate the cell morphology changes. Here, we demonstrate that myosin 1b that can mechanically link the membrane to the actin cytoskeleton interacts with EphB2 receptors via its

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Obi, Syotaro, Kimiko Yamamoto, Nobutaka Shimizu, et al. "Fluid shear stress induces arterial differentiation of endothelial progenitor cells." Journal of Applied Physiology 106, no. 1 (2009): 203–11. http://dx.doi.org/10.1152/japplphysiol.00197.2008.

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Endothelial progenitor cells (EPCs) are mobilized from bone marrow to peripheral blood and contribute to angiogenesis in tissues. In the process, EPCs are exposed to the shear stress generated by blood flow and tissue fluid flow. Our previous study showed that shear stress promotes differentiation of EPCs into mature endothelial cells. In this study, we investigated whether EPCs differentiate into arterial or venous endothelial cells in response to shear stress. When cultured EPCs derived from human peripheral blood were exposed to controlled levels of shear stress in a flow-loading device, th

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Gervais, Manon, Gwenaël Labouèbe, Alexandre Picard, Bernard Thorens, and Sophie Croizier. "EphrinB1 modulates glutamatergic inputs into POMC-expressing progenitors and controls glucose homeostasis." PLOS Biology 18, no. 11 (2020): e3000680. http://dx.doi.org/10.1371/journal.pbio.3000680.

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Proopiomelanocortin (POMC) neurons are major regulators of energy balance and glucose homeostasis. In addition to being regulated by hormones and nutrients, POMC neurons are controlled by glutamatergic input originating from multiple brain regions. However, the factors involved in the formation of glutamatergic inputs and how they contribute to bodily functions remain largely unknown. Here, we show that during the development of glutamatergic inputs, POMC neurons exhibit enriched expression of the Efnb1 (EphrinB1) and Efnb2 (EphrinB2) genes, which are known to control excitatory synapse format

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Sun, Chen-Li, Cheng-Wen Li, Nong He, et al. "Blockade of Erythropoietin-Producing Human Hepatocellular Carcinoma Receptor B1 in Spinal Dorsal Horn Alleviates Visceral Pain in Rats." Pain Research and Management 2021 (April 7, 2021): 1–9. http://dx.doi.org/10.1155/2021/7582494.

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Objective. This experiment was designed to determine whether erythropoietin-producing human hepatocellular carcinoma (Eph) receptors were involved in the development of visceral pain. Methods. Adult male Sprague-Dawley rats were randomly divided into three groups receiving different treatments (n = 16 per group): intracolonic vehicle (control group), intracolonic 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) (TNBS group), and intracolonic TNBS and intrathecal EphB1 receptor blocking reagent (TNBS + EphB2-Fc group). Visceral hyperalgesia was evaluated with quantification of visceral pain thresho

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Ghori, Adnan, Florian B. Freimann, Melina Nieminen-Kelhä, et al. "EphrinB2 Activation Enhances Vascular Repair Mechanisms and Reduces Brain Swelling After Mild Cerebral Ischemia." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 5 (2017): 867–78. http://dx.doi.org/10.1161/atvbaha.116.308620.

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Objective— Cerebral edema caused by the disruption of the blood–brain barrier is a major complication after stroke. Therefore, strategies to accelerate and enhance neurovascular recovery after stroke are of prime interest. Our main aim was to study the role of ephrinB2/EphB4 signaling in mediating the vascular repair and in blood–brain barrier restoration after mild cerebral ischemia occlusion/reperfusion. Approach and Results— Here, we show that the guidance molecule ephrinB2 plays a key role in neurovascular protection and blood–brain barrier restoration after stroke. In a focal stroke model

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Kertesz, Nathalie, Valery Krasnoperov, Ramachandra Reddy, et al. "The soluble extracellular domain of EphB4 (sEphB4) antagonizes EphB4-EphrinB2 interaction, modulates angiogenesis, and inhibits tumor growth." Blood 107, no. 6 (2006): 2330–38. http://dx.doi.org/10.1182/blood-2005-04-1655.

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AbstractThe receptor tyrosine kinase EphB4 and its ligand EphrinB2 play a crucial role in vascular development during embryogenesis. The soluble monomeric derivative of the extracellular domain of EphB4 (sEphB4) was designed as an antagonist of EphB4/EphrinB2 signaling. sEphB4 blocks activation of EphB4 and EphrinB2; suppresses endothelial cell migration, adhesion, and tube formation in vitro; and inhibits the angiogenic effects of various growth factors (VEGF and bFGF) in vivo. sEphB4 also inhibits tumor growth in murine tumor xenograft models. sEphB4 is thus a therapeutic candidate for vascu

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Ashley, George R., O. Cathal Grace, Griet Vanpoucke, and Axel A. Thomson. "Identification of EphrinB1 expression in prostatic mesenchyme and a role for EphB–EphrinB signalling in prostate development." Differentiation 80, no. 2-3 (2010): 89–98. http://dx.doi.org/10.1016/j.diff.2010.06.003.

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Liu, Rui, Runze Yu, Yuxin Cui, Mengying Fan, Bo Wang, and Yanmin Zhang. "Inhibitory effect of taspine derivative TAD1822-7 on tumor cell growth and angiogenesis via suppression of EphrinB2 and related signaling pathways." Acta Pharmaceutica 69, no. 3 (2019): 423–31. http://dx.doi.org/10.2478/acph-2019-0021.

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Abstract The aim of this study was to investigate the inhibitory effect of TAD1822-7, a synthesized taspine derivative, on cancer through its effects on tumor cell growth and angiogenesis via suppression of EphrinB2. The obtained data showed that TAD1822-7 decreased Bel-7402 cell viability and colony formation ability and suppressed cell migration. TAD1822-7 effectively inhibited blood vessel formation in an aortic ring assay to examine angiogenesis. Moreover, it also down regulated the expression of VEGFR2, VEGFR3, CD34, PLCγ, Akt, MMP2, MMP9, and CXCR4, and suppressed the expression of Ephri

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Barneh, Farnaz, Mona Moshayedi, Hamid Mirmohammadsadeghi, Shaghayegh Haghjooy-Javanmard, Ali Mohammad Sabzghabaee, and Shirinsadat Badri. "EphB4 Tyrosine Kinase Stimulation Inhibits Growth of MDA-MB-231 Breast Cancer Cells in a Dose and Time Dependent Manner." Disease Markers 35 (2013): 933–38. http://dx.doi.org/10.1155/2013/857895.

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Background. EphB4 receptor tyrosine kinase is of diagnostic and therapeutic value due to its overexpression in breast tumors. Dual functions of tumor promotion and suppression have been reported for this receptor based on presence or absence of its ligand. To elucidate such discrepancy, we aimed to determine the effect of time- and dose-dependent stimulation of EphB4 on viability and invasion of breast cancer cells via recombinant ephrinB2-Fc.Methods. Cells were seeded into multiwell plates and were stimulated by various concentrations of preclustered ephrinB2-Fc. Cell viability was measured o

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Randolph, Matthew E., Megan M. Cleary, Zia Bajwa, et al. "EphB4/EphrinB2 therapeutics in Rhabdomyosarcoma." PLOS ONE 12, no. 8 (2017): e0183161. http://dx.doi.org/10.1371/journal.pone.0183161.

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Thomas, Jacob Stephen, Heinz-Josef Lenz, Syma Iqbal, et al. "A first-in-human phase I study of sEphB4-HSA (sEphB4) with expansion in hepatocellular (HCC) and cholangiocarcinoma (CCA)." Journal of Clinical Oncology 36, no. 4_suppl (2018): 285. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.285.

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285 Background: EphrinB4, a receptor kinase, is associated with stage and survival in epithelial cancers. sEphB4 is a fusion protein of soluble EphB4 and albumin. sEphB4 binds to EphrinB2, a protein expressed in tumor cells and vessels, and blocks bidirectional signaling. sEphB4 downregulates the PI3K/AKT/mTOR pathway, inhibits angiogenesis, and promotes recruitment of cytotoxic T cells and NK cells. MTD was not reached during dose escalation. The RP2D was 10 mg/Kg weekly. Here we report the results of the expansion cohorts in HCC and CCA. Methods: The study evaluated the safety, PK, PD and ef

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Salvucci, Ombretta, Dragan Maric, Matina Economopoulou, et al. "EphrinB reverse signaling contributes to endothelial and mural cell assembly into vascular structures." Blood 114, no. 8 (2009): 1707–16. http://dx.doi.org/10.1182/blood-2008-12-192294.

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Abstract EphrinB transmembrane ligands and their cognate EphB receptor tyrosine kinases regulate vascular development through bidirectional cell-to-cell signaling, but little is known about the role of EphrinB during postnatal vascular remodeling. We report that EphrinB is a critical mediator of postnatal pericyte-to-endothelial cell assembly into vascular structures. This function is dependent upon extracellular matrix-supported cell-to-cell contact, engagement of EphrinB by EphB receptors expressed on another cell, and Src-dependent phosphorylation of the intracytoplasmic domain of EphrinB.

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Prévost, Nicolas, Donna S. Woulfe, Massimiliano Tognolini, et al. "Signaling by ephrinB1 and Eph kinases in platelets promotes Rap1 activation, platelet adhesion, and aggregation via effector pathways that do not require phosphorylation of ephrinB1." Blood 103, no. 4 (2004): 1348–55. http://dx.doi.org/10.1182/blood-2003-06-1781.

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Abstract We have previously shown that platelets express 2 receptor tyrosine kinases, EphA4 and EphB1, and the Eph kinase ligand, ephrinB1, and proposed that transcellular Eph/ephrin interactions made possible by the onset of platelet aggregation promote the further growth and stability of the hemostatic plug. The present study examines how this might occur. The results show that clustering of either ephrinB1 or EphA4 causes platelets to adhere to immobilized fibrinogen via αIIbβ3. Adhesion occurs more slowly than with adenosine diphosphate (ADP) and requires phosphatidylinositol 3 (PI3)–kinas

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Scehnet, Jeffrey S., Eric J. Ley, Valery Krasnoperov, et al. "The role of Ephs, Ephrins, and growth factors in Kaposi sarcoma and implications of EphrinB2 blockade." Blood 113, no. 1 (2009): 254–63. http://dx.doi.org/10.1182/blood-2008-02-140020.

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Abstract Kaposi sarcoma (KS) is associated with human herpesvirus (HHV)-8 and is dependent on the induction of vascular endothelial growth factors (VEGFs). VEGF regulates genes that provide arterial or venous identity to endothelial cells, such as the induction of EphrinB2, which phenotypically defines arterial endothelial cells and pericytes, and represses EphB4, which defines venous endothelial cells. We conducted a comprehensive analysis of the Eph receptor tyrosine kinases to determine which members are expressed and therefore contribute to KS pathogenesis. We demonstrated limited Eph/Ephr

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