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Journal articles on the topic 'Delta-like 4'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

Andrawes, Marie Blanke, Xiang Xu, Hong Liu, Scott B. Ficarro, Jarrod A. Marto, Jon C. Aster, and Stephen C. Blacklow. "Intrinsic Selectivity of Notch 1 for Delta-like 4 Over Delta-like 1." Journal of Biological Chemistry 288, no. 35 (July 9, 2013): 25477–89. http://dx.doi.org/10.1074/jbc.m113.454850.

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2

Fung, Erik, Sai-Man Timothy Tang, James P. Canner, Kunio Morishige, Joseph F. Arboleda-Velasquez, Angelo A. Cardoso, Nadia Carlesso, Jon C. Aster, and Masanori Aikawa. "Delta-Like 4 Induces Notch Signaling in Macrophages." Circulation 115, no. 23 (June 12, 2007): 2948–56. http://dx.doi.org/10.1161/circulationaha.106.675462.

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3

Nakano, Toshiaki, Daiju Fukuda, Jun-ichiro Koga, and Masanori Aikawa. "Delta-Like Ligand 4-Notch Signaling in Macrophage Activation." Arteriosclerosis, Thrombosis, and Vascular Biology 36, no. 10 (October 2016): 2038–47. http://dx.doi.org/10.1161/atvbaha.116.306926.

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4

Claxton, Suzanne, and Marcus Fruttiger. "Periodic Delta-like 4 expression in developing retinal arteries." Gene Expression Patterns 5, no. 1 (November 2004): 123–27. http://dx.doi.org/10.1016/j.modgep.2004.05.004.

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5

Luca, V. C., K. M. Jude, N. W. Pierce, M. V. Nachury, S. Fischer, and K. C. Garcia. "Structural basis for Notch1 engagement of Delta-like 4." Science 347, no. 6224 (February 19, 2015): 847–53. http://dx.doi.org/10.1126/science.1261093.

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6

Yan, M., and G. D. Plowman. "Delta-like 4/Notch Signaling and Its Therapeutic Implications." Clinical Cancer Research 13, no. 24 (December 15, 2007): 7243–46. http://dx.doi.org/10.1158/1078-0432.ccr-07-1393.

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7

Yu, Yi, Yang Zhao, Guangming Zhou, and Xiang Wang. "Therapeutic Efficacy of Delta-Like Ligand 4 Gene Vaccine Overexpression on Liver Cancer in Mice." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382094220. http://dx.doi.org/10.1177/1533033820942205.

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Delta-like ligand 4 is a notch ligand that is predominantly expressed in the endothelial tip cells and plays essential roles in the regulation of angiogenesis. In this study, we explored the therapeutic effects of delta-like ligand 4 gene vaccine overexpression on the syngeneic model mouse model of liver cancer and the underlying mechanisms. Mouse hepatocellular carcinoma cell line H22-H8D8 was used to generate subcutaneous syngeneic model liver cancer in Kunming mice, and the effects of recombinant plasmid pVAX1 containing delta-like ligand 4 vaccine on tumor growth was examined. Compared to controls, delta-like ligand 4 vaccination reduced syngeneic model tumor size by 70.31% (from 17.11 ± 9.30 cm3 to 5.08 ± 2.75 cm3, P = .035) and tumor weight by 34.19% (from 6.26 ± 3.01 g to 4.12 ± 2.52 g, P = .102), while the mouse survival was significantly increased (from 27.7 ± 6.0 days to 33.1 ± 6.1 days, P = .047). High level of delta-like ligand 4 antibody, together with a significantly increased number of CD4+ and decreased CD8+ cells were identified in the mouse peripheral blood serum samples after delta-like ligand 4 immunization. In addition, elevated serum levels of interleukin 2, interleukin 4, and interferon γ were detected in the delta-like ligand 4–vaccinated mice when compared to the controls. Further studies have revealed increased CD31 and decreased Ki67 expression in the syngeneic model tumor tissues of vaccinated mice. Taken together, our studies suggest that delta-like ligand 4 gene vaccine can inhibit the growth of hepatocellular carcinoma in mice through inhibiting tumor angiogenesis and boosting antitumor immune responses. Hence, delta-like ligand 4 gene vaccination may be a promising strategy for the treatment of transplanted liver cancer.

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8

Liu, Ya-Rong, Ying-Yun Guan, Xin Luan, Qin Lu, Chao Wang, Hai-Jun Liu, Yun-Ge Gao, et al. "Delta-like ligand 4-targeted nanomedicine for antiangiogenic cancer therapy." Biomaterials 42 (February 2015): 161–71. http://dx.doi.org/10.1016/j.biomaterials.2014.11.039.

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9

Liu, Stanley K., Saif A. S. Bham, Emmanouil Fokas, John Beech, Jaehong Im, Song Cho, Adrian L. Harris, and Ruth J. Muschel. "Delta-Like Ligand 4–Notch Blockade and Tumor Radiation Response." JNCI: Journal of the National Cancer Institute 103, no. 23 (December 7, 2011): 1778–98. http://dx.doi.org/10.1093/jnci/djr419.

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10

Mazella, J., S. Liang, and L. Tseng. "Expression of Delta-Like Protein 4 in the Human Endometrium." Endocrinology 149, no. 1 (October 4, 2007): 15–19. http://dx.doi.org/10.1210/en.2007-0477.

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Activation of Delta-Notch signaling pathway promotes the development of the vascular system in embryo, normal adult tissues, and cancerous lesions. Delta and Notch genes are known to be expressed in endothelial cells, and little is known of their expression beyond the vascular system. The purpose of this study was to investigate whether Delta gene would be expressed in cells of the uterine endometrium. In this study, we found that the human endometrial cells expressed one of the Delta ligands, Delta-like 4 protein (Dll4). Dll4 was expressed in human endometrium in a spatiotemporal fashion. Immunohistochemistry studies showed the cytoplasm as well as membrane staining with apical localization both in the luminal and glandular epithelium and moderate diffuse staining in the cytoplasm of the stromal cells. Western blot analysis showed that the size of the endometrial Dll4 was identical to that in the human umbilical endothelial cells. The expression of Dll4 mRNA in human endometrial cells was quantitatively determined by real-time PCR. Dll4 mRNA expressed in the glandular epithelium showed large variations, and it was significantly elevated in the mid and late proliferative and early secretory endometrium. Endometrial stromal cells contained less Dll4 mRNA and had no clear correlation with the menstrual cycle. The effect of hormones was studied in the primary culture of isolated glandular epithelial and stromal cells. In glandular cells, estradiol had little effect, and medroxyprogesterone acetate significantly reduced the mRNAs compared with that of control. Relaxin induced the Dll4 mRNA. In stromal cells, both estradiol and medroxyprogesterone acetate reduced the Dll4 mRNA. To our knowledge, this is the first report of the expression of Dll4 in the endometrium. We propose that endometrial Dll4 may enhance the development of the endometrial microvascular system and facilitate the implantation of blastocyst in a fertile cycle.

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11

Van de Walle, Inge, Greet De Smet, Martina Gärtner, Magda De Smedt, Els Waegemans, Bart Vandekerckhove, Georges Leclercq, et al. "Jagged2 acts as a Delta-like Notch ligand during early hematopoietic cell fate decisions." Blood 117, no. 17 (April 28, 2011): 4449–59. http://dx.doi.org/10.1182/blood-2010-06-290049.

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Abstract Notch signaling critically mediates various hematopoietic lineage decisions and is induced in mammals by Notch ligands that are classified into 2 families, Delta-like (Delta-like-1, -3 and -4) and Jagged (Jagged1 and Jagged2), based on structural homology with both Drosophila ligands Delta and Serrate, respectively. Because the functional differences between mammalian Notch ligands were still unclear, we have investigated their influence on early human hematopoiesis and show that Jagged2 affects hematopoietic lineage decisions very similarly as Delta-like-1 and -4, but very different from Jagged1. OP9 coculture experiments revealed that Jagged2, like Delta-like ligands, induces T-lineage differentiation and inhibits B-cell and myeloid development. However, dose-dependent Notch activation studies, gene expression analysis, and promoter activation assays indicated that Jagged2 is a weaker Notch1-activator compared with the Delta-like ligands, revealing a Notch1 specific signal strength hierarchy for mammalian Notch ligands. Strikingly, Lunatic-Fringe– mediated glycosylation of Notch1 potentiated Notch signaling through Delta-like ligands and also Jagged2, in contrast to Jagged1. Thus, our results reveal a unique role for Jagged1 in preventing the induction of T-lineage differentiation in hematopoietic stem cells and show an unexpected functional similarity between Jagged2 and the Delta-like ligands.

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12

Huang, Qing Bo, Xin Ma, Hong Zhao Li, Qing Ai, Shang Wen Liu, Yu Zhang, Yu Gao, et al. "Endothelial Delta-like 4 (DLL4) promotes renal cell carcinoma hematogenous metastasis." Oncotarget 5, no. 10 (March 14, 2014): 3066–75. http://dx.doi.org/10.18632/oncotarget.1827.

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13

Shen, Z., Y. Liu, J. Hu, O. Park, T. Feng, B. Dewidar, C. Xu, et al. "P0430 : Delta like ligand 4 drives liver damage through regulating chemokines." Journal of Hepatology 62 (April 2015): S474. http://dx.doi.org/10.1016/s0168-8278(15)30640-1.

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14

Koga, Jun-ichiro, Toshiaki Nakano, James E. Dahlman, Jose-Luiz Figueiredo, Hengmin Zhang, Julius Decano, Omar F. Khan, et al. "Macrophage Notch Ligand Delta-Like 4 Promotes Vein Graft Lesion Development." Arteriosclerosis, Thrombosis, and Vascular Biology 35, no. 11 (November 2015): 2343–53. http://dx.doi.org/10.1161/atvbaha.115.305516.

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15

Mohtashami, Mahmood, Divya K. Shah, Korosh Kianizad, Geneve Awong, and Juan Carlos Zúñiga-Pflücker. "Induction of T-cell development by Delta-like 4-expressing fibroblasts." International Immunology 25, no. 10 (August 29, 2013): 601–11. http://dx.doi.org/10.1093/intimm/dxt027.

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16

Masuda, S. "Re: Delta-Like Ligand 4-Notch Blockade and Tumor Radiation Response." JNCI Journal of the National Cancer Institute 104, no. 5 (January 20, 2012): 421. http://dx.doi.org/10.1093/jnci/djs006.

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17

Leslie, J. D., L. Ariza-McNaughton, A. L. Bermange, R. McAdow, S. L. Johnson, and J. Lewis. "Endothelial signalling by the Notch ligand Delta-like 4 restricts angiogenesis." Development 134, no. 5 (January 24, 2007): 839–44. http://dx.doi.org/10.1242/dev.003244.

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18

Fukuda, D., E. Aikawa, F. K. Swirski, T. I. Novobrantseva, V. Kotelianski, C. Z. Gorgun, A. Chudnovskiy, et al. "Notch ligand Delta-like 4 blockade attenuates atherosclerosis and metabolic disorders." Proceedings of the National Academy of Sciences 109, no. 27 (June 13, 2012): E1868—E1877. http://dx.doi.org/10.1073/pnas.1116889109.

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19

Liu, S. K., R. J. Muschel, and A. L. Harris. "Response: Re: Delta-Like Ligand 4-Notch Blockade and Tumor Radiation Response." JNCI Journal of the National Cancer Institute 104, no. 5 (January 20, 2012): 421–22. http://dx.doi.org/10.1093/jnci/djs007.

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20

Al Haj Zen, Ayman, Atsuhiko Oikawa, Miriam Bazan-Peregrino, Marco Meloni, Costanza Emanueli, and Paolo Madeddu. "Inhibition of Delta-Like-4–Mediated Signaling Impairs Reparative Angiogenesis After Ischemia." Circulation Research 107, no. 2 (July 23, 2010): 283–93. http://dx.doi.org/10.1161/circresaha.110.221663.

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21

Schaller, Matthew A., Hannah Logue, Sumanta Mukherjee, Dennis M. Lindell, Ana Lucia Coelho, Pamela Lincoln, William F. Carson, et al. "Delta-Like 4 Differentially Regulates Murine CD4+ T Cell Expansion via BMI1." PLoS ONE 5, no. 8 (August 17, 2010): e12172. http://dx.doi.org/10.1371/journal.pone.0012172.

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22

Shen, Zhe, Yan Liu, Bedair Dewidar, Junhao Hu, Ogyi Park, Teng Feng, Chengfu Xu, et al. "Delta-Like Ligand 4 Modulates Liver Damage by Down-Regulating Chemokine Expression." American Journal of Pathology 186, no. 7 (July 2016): 1874–89. http://dx.doi.org/10.1016/j.ajpath.2016.03.010.

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23

Wiseman, John, Pernilla Gregersson, Johan Johansson, Kerstin Magnell, Fernanda Pilataxi, Chris Morehouse, Philip Brohawn, Nicholas Holoweckyj, Patrick Strout, and Song Cho. "Generation of a functional humanized Delta-like ligand 4 transgenic mouse model." Transgenic Research 26, no. 6 (August 17, 2017): 791–98. http://dx.doi.org/10.1007/s11248-017-0040-3.

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24

Tsukamoto, Noriyuki, Manami Itoi, Mitsuo Nishikawa, and Takashi Amagai. "Lack of Delta like 1 and 4 expressions in nude thymus anlages." Cellular Immunology 234, no. 2 (April 2005): 77–80. http://dx.doi.org/10.1016/j.cellimm.2005.06.009.

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25

Yamanda, Shinsuke, Satoru Ebihara, Masanori Asada, Tatsuma Okazaki, Kaijun Niu, Takae Ebihara, Akemi Koyanagi, Noriko Yamaguchi, Hideo Yagita, and Hiroyuki Arai. "Role of ephrinB2 in nonproductive angiogenesis induced by Delta-like 4 blockade." Blood 113, no. 15 (April 9, 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 tumor growth and induced nonproductive angiogenesis. DLL4 was expressed in subcutaneous tumors, and DLL4 blockade suppressed ephrinB2 expression in the tumors. DLL4 blockade significantly promoted human umbilical vein endothelial cell (HUVEC) proliferation in vitro, and the effect was additive to that of VEGF. Both DLL4 blockade and VEGF significantly increased cord length and branch points in a tubular formation assay. Expression of ephrinB2 in HUVECs was enhanced by VEGF alone, and the enhancement was inhibited by DLL4 blockade. Moreover, when we studied the effect of ephrinB2 RNA interference on HUVEC tubular formation, knockdown of ephrinB2 mimicked the effect of DLL4. These results suggest that ephrinB2 plays a crucial role in nonproductive angiogenesis caused by DLL4 blockade.

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26

Oon, Chern Ein, Esther Bridges, Helen Sheldon, Richard C. A. Sainson, Adrian Jubb, Helen Turley, Russell Leek, Francesca Buffa, Adrian L. Harris, and Ji-Liang Li. "Role of Delta-like 4 in Jagged1-induced tumour angiogenesis and tumour growth." Oncotarget 8, no. 25 (April 8, 2017): 40115–31. http://dx.doi.org/10.18632/oncotarget.16969.

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27

Fiorini, Emma, Isabel Ferrero, Estelle Merck, Stéphanie Favre, Michel Pierres, Sanjiv A. Luther, and H. Robson MacDonald. "Cutting Edge: Thymic Crosstalk Regulates Delta-Like 4 Expression on Cortical Epithelial Cells." Journal of Immunology 181, no. 12 (December 2, 2008): 8199–203. http://dx.doi.org/10.4049/jimmunol.181.12.8199.

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28

Hozumi, Katsuto, Carolina Mailhos, Naoko Negishi, Ken-ichi Hirano, Takashi Yahata, Kiyoshi Ando, Saulius Zuklys, Georg A. Holländer, David T. Shima, and Sonoko Habu. "Delta-like 4 is indispensable in thymic environment specific for T cell development." Journal of Experimental Medicine 205, no. 11 (September 29, 2008): 2507–13. http://dx.doi.org/10.1084/jem.20080134.

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The thymic microenvironment is required for T cell development in vivo. However, in vitro studies have shown that when hematopoietic progenitors acquire Notch signaling via Delta-like (Dll)1 or Dll4, they differentiate into the T cell lineage in the absence of a thymic microenvironment. It is not clear, however, whether the thymus supports T cell development specifically by providing Notch signaling. To address this issue, we generated mice with a loxP-flanked allele of Dll4 and induced gene deletion specifically in thymic epithelial cells (TECs). In the thymus of mutant mice, the expression of Dll4 was abrogated on the epithelium, and the proportion of hematopoietic cells bearing the intracellular fragment of Notch1 (ICN1) was markedly decreased. Corresponding to this, CD4 CD8 double-positive or single-positive T cells were not detected in the thymus. Further analysis showed that the double-negative cell fraction was lacking T cell progenitors. The enforced expression of ICN1 in hematopoietic progenitors restored thymic T cell differentiation, even when the TECs were deficient in Dll4. These results indicate that the thymus-specific environment for determining T cell fate indispensably requires Dll4 expression to induce Notch signaling in the thymic immigrant cells.

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29

Hozumi, Katsuto, Carolina Mailhos, Naoko Negishi, Ken-ichi Hirano, Takashi Yahata, Kiyoshi Ando, Saulius Zuklys, Georg A. Holländer, David T. Shima, and Sonoko Habu. "Delta-like 4 is indispensable in thymic environment specific for T cell development." Journal of Cell Biology 183, no. 1 (October 6, 2008): i2. http://dx.doi.org/10.1083/jcb1831oia2.

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30

Hu, W., C. Lu, R. Stone, J. Bottsford-Miller, A. Nick, M. Shahzad, K. Matsuo, R. Coleman, and A. Sood. "Biologic roles of tumor and endothelial delta-like ligand 4 in ovarian cancer." Gynecologic Oncology 120 (March 2011): S35—S36. http://dx.doi.org/10.1016/j.ygyno.2010.12.087.

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31

Real, Carla, Francisco Caiado, Catia Igreja, Ana P. Elias, Cristina Borges, Antonio Duarte, and Sergio Dias. "Delta Like 4 Expressing Bone Marrow-Derived Endothelial Progenitor Cells Regulate Tumour Angiogenesis." Blood 110, no. 11 (November 16, 2007): 3728. http://dx.doi.org/10.1182/blood.v110.11.3728.3728.

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Abstract Bone marrow-derived endothelial progenitor cells (BM-EPCs) have been implicated in adult neoangiogenesis and consequently used as therapies for human pathologies with endothelial damage. The administration of these cells in human patients temporally improves endothelial function, although the engraftment of these cells in newly formed vessels is inefficient. Conversely, therapeutic stratagies to block EPC contribution during tumor angiogenesis have been proposed. In this work, we analysed the role of the Notch/Delta signalling pathway in EPC function during tumour neoangiogenesis, by regulating the expression of Notch ligand, delta-like 4 (Dll4) in these cells. Sublethally irradiated NOD-SCID mice received WT, Dll4+/− (Dll4 heterozygous mice) or Dll4 SiRNA-treated BM-EPCs and were subcutaneously inoculated with well established Human or murine tumor xenografts. Tumours growing in Dll4-depleted EPCs transplanted mice presented increased microvessel density when compared with WT EPCs transplanted mice or non-transplanted controls, regardless of VEGF expression. Although with increased vessel number, tumours of Dll4+/− EPC transplanted mice presented increased hypoxia and decreased tumour cell proliferation, suggesting an impairment in vessel function. In addition, these tumours present a diminished expression of PDGF, a vessel stabilizing factor, and increased expression of Ang2, known as a vessel destabilizing factor. We next verified whether the vessel destabilization observed in tumors after Dll4-depleted EPCs transplant might be due to a diferential endothelial differentiation or incorporation of EPCs in the tumour vasculature. In order to answer this question we quantified the incorporation of WT and Dll4-depleted EPCs in tumour vessels. Accordingly to our results, the presence of Dll4-depleted EPCs was reduced compared to WT EPCs, suggesting that Dll4-depleted EPCs might have reduced capacity to adhere to the renewing tumor vasculature, or to the underlying basement membrane. To test this, we used an in vitro endothelial differentiation assay, and observed a defect on the adhesion of of Dll4-depleted EPCs to extracellular matrix, which was correlated with a reduced expression of integrin subunits a3 and b1. These results suggest that the reduction of Dll4 on EPCs reduces integrin expression interfering with their ability to adhere, incorporate and stabilize the tumor vasculature during tumor neoangiogenesis. Therefore, EPCs have a major role in vessel stabilization in active neoangiogenic sites by the regulation of Dll4 expression. We propose that targeting the Notch/Dll4 pathway on EPCs, modulating vessel stability, may have therapeutic potential.

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32

Real, Carla, Leonor Remédio, Francisco Caiado, Cátia Igreja, Cristina Borges, Alexandre Trindade, Perpétua Pinto-do-Ó, Hideo Yagita, Antonio Duarte, and Sérgio Dias. "Bone Marrow-Derived Endothelial Progenitors Expressing Delta-Like 4 (Dll4) Regulate Tumor Angiogenesis." PLoS ONE 6, no. 4 (April 4, 2011): e18323. http://dx.doi.org/10.1371/journal.pone.0018323.

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33

Williams, Cassin Kimmel, Marta Segarra, Maria De La Luz Sierra, Richard C. A. Sainson, Giovanna Tosato, and Adrian L. Harris. "Regulation of CXCR4 by the Notch Ligand Delta-like 4 in Endothelial Cells." Cancer Research 68, no. 6 (March 13, 2008): 1889–95. http://dx.doi.org/10.1158/0008-5472.can-07-2181.

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34

Jubb, Adrian M., Lisa Browning, Leticia Campo, Helen Turley, Graham Steers, Gavin Thurston, Adrian L. Harris, and Olaf Ansorge. "Expression of vascular Notch ligands Delta-like 4 and Jagged-1 in glioblastoma." Histopathology 60, no. 5 (February 1, 2012): 740–47. http://dx.doi.org/10.1111/j.1365-2559.2011.04138.x.

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35

Ishida, Waka, Ken Fukuda, Shuji Sakamoto, Noriko Koyama, Akemi Koyanagi, Hideo Yagita, and Atsuki Fukushima. "Regulation of Experimental Autoimmune Uveoretinitis by Anti-Delta-Like Ligand 4 Monoclonal Antibody." Investigative Opthalmology & Visual Science 52, no. 11 (October 17, 2011): 8224. http://dx.doi.org/10.1167/iovs.11-7756.

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36

Luo, Qingqing, Wen Zhang, Xiaoxia Liu, Yanfang Zheng, Hui Gao, Yin Zhao, and Li Zou. "Delta-Like 4-Notch signaling regulates trophoblast migration and invasion by targeting EphrinB2." Biochemical and Biophysical Research Communications 527, no. 4 (July 2020): 915–21. http://dx.doi.org/10.1016/j.bbrc.2020.05.032.

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37

Subramanyan, Ram Kumar, Loubna Hassanieh, Jasbir Singh, Parkash Gill, and Fred Weaver. "Delta-like ligand-4 induces angiogenesis at sites of neovascularization in the adult." Journal of the American College of Surgeons 203, no. 3 (September 2006): S100—S101. http://dx.doi.org/10.1016/j.jamcollsurg.2006.05.264.

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38

Ting, Hung-An, Matthew A. Schaller, Denise E. de Almeida Nagata, Andrew J. Rasky, Ivan P. Maillard, and Nicholas W. Lukacs. "Notch Ligand Delta-like 4 Promotes Regulatory T Cell Identity in Pulmonary Viral Infection." Journal of Immunology 198, no. 4 (January 11, 2017): 1492–502. http://dx.doi.org/10.4049/jimmunol.1601654.

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39

Jubb, Adrian M., Elizabeth J. Soilleux, Helen Turley, Graham Steers, Andrew Parker, Irene Low, Jennifer Blades, et al. "Expression of Vascular Notch Ligand Delta-Like 4 and Inflammatory Markers in Breast Cancer." American Journal of Pathology 176, no. 4 (April 2010): 2019–28. http://dx.doi.org/10.2353/ajpath.2010.090908.

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40

Geers, Caroline, Ides M. Colin, and Anne-Catherine Gérard. "Delta-Like 4/Notch Pathway Is Differentially Regulated in Benign and Malignant Thyroid Tissues." Thyroid 21, no. 12 (December 2011): 1323–30. http://dx.doi.org/10.1089/thy.2010.0444.

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41

Fukuda, Daiju, and Masanori Aikawa. "Expanding Role of Delta-Like 4 Mediated Notch Signaling in Cardiovascular and Metabolic Diseases." Circulation Journal 77, no. 10 (2013): 2462–68. http://dx.doi.org/10.1253/circj.cj-13-0873.

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42

Schott, M., and A. Thiel. "Delta-Like 4/Notch Pathway Is Differentially Regulated in Benign and Malignant Thyroid Tissues." Yearbook of Endocrinology 2012 (January 2012): 179–81. http://dx.doi.org/10.1016/j.yend.2012.04.029.

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43

Jubb, A. M., H. Turley, H. C. Moeller, G. Steers, C. Han, J.-L. Li, R. Leek, et al. "Expression of delta-like ligand 4 (Dll4) and markers of hypoxia in colon cancer." British Journal of Cancer 101, no. 10 (October 20, 2009): 1749–57. http://dx.doi.org/10.1038/sj.bjc.6605368.

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44

Laranjeiro, Ricardo, Isabel Alcobia, Hélia Neves, Andreia C. Gomes, Pedro Saavedra, Catarina C. Carvalho, António Duarte, António Cidadão, and Leonor Parreira. "The Notch Ligand Delta-Like 4 Regulates Multiple Stages of Early Hemato-Vascular Development." PLoS ONE 7, no. 4 (April 13, 2012): e34553. http://dx.doi.org/10.1371/journal.pone.0034553.

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45

Wang, Q., Y. Shi, HJ Butler, J. Xue, G. Wang, P. Duan, and H. Zheng. "Role of delta-like ligand-4 in chemoresistance against docetaxel in MCF-7 cells." Human & Experimental Toxicology 36, no. 4 (June 22, 2016): 328–38. http://dx.doi.org/10.1177/0960327116650006.

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As Notch receptors have been shown to induce chemoresistance, we hypothesized that delta-like ligand-4 (DLL4), a central Notch signalling ligand, might also participate in chemoresistance in breast cancer. To investigate this issue, overexpression of DLL4 was induced by transfection with expression vectors for DLL4 in the human breast cancer cell line Michigan cancer foundation-7 (MCF-7). It was found that DLL4 could be adaptively upregulated by docetaxel (DOC) treatment in a dose-dependent manner, but Notch1 was unaffected. Overexpression of DLL4 could significantly attenuate the cytotoxic effects of DOC by increasing Bcl-2 expression, while decreasing Bax expression, apoptosis rate and DNA damage. The protective effects of DLL4 made cells acquire chemoresistance against DOC and resulted in cancer cell survival. DLL4 is normally regarded as a regulator of vascular development. Our results expanded the understanding of DLL4. Since DLL4 may play an important role in the process of acquiring chemoresistance, it may be a promising target in overcoming chemoresistance in breast cancer.

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46

Billiard, Fabienne, Sevasti Karaliota, Bei Wang, Dimitrios Stellas, Ioannis Serafimidis, Antigoni Manousopoulou, Yiassemi Koutmani, et al. "Delta-like Ligand-4-Notch Signaling Inhibition Regulates Pancreatic Islet Function and Insulin Secretion." Cell Reports 22, no. 4 (January 2018): 895–904. http://dx.doi.org/10.1016/j.celrep.2017.12.076.

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Camelo, Serge, William Raoul, Sophie Lavalette, Bertrand Calippe, Brunella Cristofaro, Olivier Levy, Marianne Houssier, et al. "Delta-like 4 inhibits choroidal neovascularization despite opposing effects on vascular endothelium and macrophages." Angiogenesis 15, no. 4 (August 7, 2012): 609–22. http://dx.doi.org/10.1007/s10456-012-9290-0.

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48

Mizuno, K., K. Hasegawa, T. Katagiri, M. Ogimoto, T. Ichikawa, and H. Yakura. "MPTP delta, a putative murine homolog of HPTP delta, is expressed in specialized regions of the brain and in the B-cell lineage." Molecular and Cellular Biology 13, no. 9 (September 1993): 5513–23. http://dx.doi.org/10.1128/mcb.13.9.5513.

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Protein tyrosine phosphatases (PTPs), together with protein tyrosine kinases (PTKs), are involved in the regulation of cell activation, growth, and differentiation. To further elucidate the fine tuning of cell growth and differentiation through tyrosine phosphorylation, we tried to isolate mouse receptor-type PTP (RPTP) cDNA clones by screening mouse brain cDNA libraries with mouse CD45 PTP domain probes under reduced-stringency conditions. Characterization of isolated cDNA clones for RPTP showed that the cytoplasmic region contains two tandem repeats of PTP domain of about 230 amino acids with intrinsic phosphatase activity. The extracellular region was composed of immunoglobulin (Ig)-like domains and fibronectin type III (FN-III)-like domains. The gene was highly homologous to human PTP delta (HPTP delta) and thus was named MPTP delta (murine counterpart of HPTP delta). The MPTP delta gene appeared to generate at least three species of mRNA, which differ in the composition of the extracellular domain: type A, one Ig-like and four FN-III-like domains; type B, one Ig-like and eight FN-III-like domains; and type C, three Ig-like and eight FN-III-like domains. Interestingly, the 5' untranslated region and the leader peptide of types A and B were completely different from those of type C. Northern (RNA) blot analysis demonstrated that brain, kidney, and heart cells express three mRNA species of about 7 kb. Antibody directed against part of the extracellular domain of type A MPTP delta recognized a 210-kDa protein in brain and kidney lysates. In situ hybridization of brain samples revealed that MPTP delta mRNA is present in the hippocampus, thalamic reticular nucleus, and piriform cortex, where some Src family PTKs have been also demonstrated to exist. Although MPTP delta mRNA was not detected in lymphoid tissues, all of the pre-B-cell lines tested and one of three B-cell lines tested expressed MPTP delta mRNA, whereas antibody-producing B-cell hybridomas and T-cell and macrophage lines did not. Finally, the MPTP delta locus was tightly linked to the brown (b) locus on mouse chromosome 4.

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49

Mizuno, K., K. Hasegawa, T. Katagiri, M. Ogimoto, T. Ichikawa, and H. Yakura. "MPTP delta, a putative murine homolog of HPTP delta, is expressed in specialized regions of the brain and in the B-cell lineage." Molecular and Cellular Biology 13, no. 9 (September 1993): 5513–23. http://dx.doi.org/10.1128/mcb.13.9.5513-5523.1993.

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Abstract:

Protein tyrosine phosphatases (PTPs), together with protein tyrosine kinases (PTKs), are involved in the regulation of cell activation, growth, and differentiation. To further elucidate the fine tuning of cell growth and differentiation through tyrosine phosphorylation, we tried to isolate mouse receptor-type PTP (RPTP) cDNA clones by screening mouse brain cDNA libraries with mouse CD45 PTP domain probes under reduced-stringency conditions. Characterization of isolated cDNA clones for RPTP showed that the cytoplasmic region contains two tandem repeats of PTP domain of about 230 amino acids with intrinsic phosphatase activity. The extracellular region was composed of immunoglobulin (Ig)-like domains and fibronectin type III (FN-III)-like domains. The gene was highly homologous to human PTP delta (HPTP delta) and thus was named MPTP delta (murine counterpart of HPTP delta). The MPTP delta gene appeared to generate at least three species of mRNA, which differ in the composition of the extracellular domain: type A, one Ig-like and four FN-III-like domains; type B, one Ig-like and eight FN-III-like domains; and type C, three Ig-like and eight FN-III-like domains. Interestingly, the 5' untranslated region and the leader peptide of types A and B were completely different from those of type C. Northern (RNA) blot analysis demonstrated that brain, kidney, and heart cells express three mRNA species of about 7 kb. Antibody directed against part of the extracellular domain of type A MPTP delta recognized a 210-kDa protein in brain and kidney lysates. In situ hybridization of brain samples revealed that MPTP delta mRNA is present in the hippocampus, thalamic reticular nucleus, and piriform cortex, where some Src family PTKs have been also demonstrated to exist. Although MPTP delta mRNA was not detected in lymphoid tissues, all of the pre-B-cell lines tested and one of three B-cell lines tested expressed MPTP delta mRNA, whereas antibody-producing B-cell hybridomas and T-cell and macrophage lines did not. Finally, the MPTP delta locus was tightly linked to the brown (b) locus on mouse chromosome 4.

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Reimann, Christian, Liliane Dal-Cortivo, Brigitte Ternaux, Emmanuelle Six, Julien Rouiller, Marina Cavazzana-Calvo, and Isabelle Andre-Schmutz. "In Vitro Generation of Human T-Cell Precursors From Bone Marrow CD34+ Cells by Short Exposure to Immobilized Notch-Ligand Delta-Like 4." Blood 114, no. 22 (November 20, 2009): 3532. http://dx.doi.org/10.1182/blood.v114.22.3532.3532.

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Abstract Abstract 3532 Poster Board III-469 Prolonged posttransplant immune deficiency is a major complication following hematopoietic stem cell transplantation, particularly in the T-lymphoid compartment. Accelerating T-cell development by injecting donor derived T-cell precursors has been proposed as a novel strategy to shorten the immune deficient phase. Several research groups have successfully generated T-cell precursors from murine and human HSC in vitro by transitory exposure to the Notch-ligand presenting murine OP9DL1-cell line. Transfer of the in vitro generated murine T-cell precursors into irradiated NOD/SCID/γcnull-mice accelerated T-cellular reconstitution. However, the clinical application of the OP9DL1-system is limited. Recent studies have demonstrated that short exposure of cord blood CD34+ cells to Notch-ligand Delta-like 4 is sufficient to promote human T-cell differentiation in vitro. Here, we modified this technique to better characterize and ameliorate T-cell development in vitro, with the objective of eventually transferring this method to a clinical phase. Towards this aim, we exposed human CD34+ HSC derived from any available source to immobilized Notch-ligand Delta-like 4 in the presence of different cytokine combinations implicated in human haematopoiesis (IL-7, SCF, Flt3-ligand and TPO). Within 7 days a population of CD34+CD7+ and CD34-CD7++ T-cell precursors emerged in the presence of Delta-like 4, but not under control conditions. After 7 days the CD34+CD7+ population subsequently declined while further amplification of the CD34-CD7++ population was observed. Two distinct progenitor subsets emerged within the CD34-CD7++ population, namely CD34-CD7++CD5+ and CD34-CD7++CD5-. The CD34-CD7++CD5+ subset further acquired CD1a and, thus, adopted a pre-T-cell phenotype. Between days 7 and 14 the CD34-CD7++CD5- acquired a NK-cell phenotype, as indicated by CD16 and CD56 expression. Beyond 14 days no further expansion of the pre-T-cell fraction was observed, while the NK-cell fraction continued proliferating. More advanced stages T-cell development, such as immature single positive CD4+ cells as observable in OP9DL1 co-cultures, did not arise after exposing cells only to immobilized Delta-like4. Intermittent emergence of a CD13+CD14+CD7- myeloid population was observed within the first 14 days of culture on Delta-like 4; however, this population disappeared spontaneously and did not preserve its common myeloid progenitor. Selecting a more immature CD34+CD38- population resulted in a two-fold increase of the frequency of CD34+CD7+ and CD34-CD7++ cells as compared to the whole CD34+ population, while myeloid differentiation was inhibited. A further increase was obtained by replanting cultured cells to freshly coated plates with Delta-like 4 every 3 days of culture. T-cell precursors cells derived after 7 days of culture were injected into NOD/SCID/γcnull mice. The in vivo-experiments are ongoing and results are pending. Our results provide further evidence that human T-cell precursors can be generated in vitro, not only in co-culture with murine OP9DL1-cells but also by short exposure to immobilized Notch-ligand Delta-like 4. These ongoing experiments are an important prerequisite for the potential clinical application of this method. Disclosures: No relevant conflicts of interest to declare.

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