Relevant bibliographies by topics / Lumen Morphogenesis

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Lumen Morphogenesis'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Lumen Morphogenesis"

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Herrema, Hilde, Dominika Czajkowska, Delphine Théard, Johanna M. van der Wouden, Dharamdajal Kalicharan, Behnam Zolghadr, Dick Hoekstra, and Sven C. D. van IJzendoorn. "Rho Kinase, Myosin-II, and p42/44 MAPK Control Extracellular Matrix-mediated Apical Bile Canalicular Lumen Morphogenesis in HepG2 Cells." Molecular Biology of the Cell 17, no. 7 (July 2006): 3291–303. http://dx.doi.org/10.1091/mbc.e06-01-0067.

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The molecular mechanisms that regulate multicellular architecture and the development of extended apical bile canalicular lumens in hepatocytes are poorly understood. Here, we show that hepatic HepG2 cells cultured on glass coverslips first develop intercellular apical lumens typically formed by a pair of cells. Prolonged cell culture results in extensive organizational changes, including cell clustering, multilayering, and apical lumen morphogenesis. The latter includes the development of large acinar structures and subsequent elongated canalicular lumens that span multiple cells. These morphological changes closely resemble the early organizational pattern during development, regeneration, and neoplasia of the liver and are rapidly induced when cells are cultured on predeposited extracellular matrix (ECM). Inhibition of Rho kinase or its target myosin-II ATPase in cells cultured on glass coverslips mimics the morphogenic response to ECM. Consistently, stimulation of Rho kinase and subsequent myosin-II ATPase activity by lipoxygenase-controlled eicosatetranoic acid metabolism inhibits ECM-mediated cell multilayering and apical lumen morphogenesis but not initial apical lumen formation. Furthermore, apical lumen remodeling but not cell multilayering requires basal p42/44 MAPK activity. Together, the data suggest a role for hepatocyte-derived ECM in the spatial organization of hepatocytes and apical lumen morphogenesis and identify Rho kinase, myosin-II, and MAPK as potentially important players in different aspects of bile canalicular lumen morphogenesis.
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Datta, Anirban, David M. Bryant, and Keith E. Mostov. "Molecular Regulation of Lumen Morphogenesis." Current Biology 21, no. 3 (February 2011): R126—R136. http://dx.doi.org/10.1016/j.cub.2010.12.003.

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Enemchukwu, Nduka O., Ricardo Cruz-Acuña, Tom Bongiorno, Christopher T. Johnson, José R. García, Todd Sulchek, and Andrés J. García. "Synthetic matrices reveal contributions of ECM biophysical and biochemical properties to epithelial morphogenesis." Journal of Cell Biology 212, no. 1 (December 28, 2015): 113–24. http://dx.doi.org/10.1083/jcb.201506055.

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Epithelial cells cultured within collagen and laminin gels proliferate to form hollow and polarized spherical structures, recapitulating the formation of a rudimentary epithelial organ. However, the contributions of extracellular matrix (ECM) biochemical and biophysical properties to morphogenesis are poorly understood because of uncontrolled presentation of multiple adhesive ligands, limited control over mechanical properties, and lot-to-lot compositional variability in these natural ECMs. We engineered synthetic ECM-mimetic hydrogels with independent control over adhesive ligand density, mechanical properties, and proteolytic degradation to study the impact of ECM properties on epithelial morphogenesis. Normal cyst growth, polarization, and lumen formation were restricted to a narrow range of ECM elasticity, whereas abnormal morphogenesis was observed at lower and higher elastic moduli. Adhesive ligand density dramatically regulated apicobasal polarity and lumenogenesis independently of cell proliferation. Finally, a threshold level of ECM protease degradability was required for apicobasal polarity and lumen formation. This synthetic ECM technology provides new insights into how cells transduce ECM properties into complex morphogenetic behaviors.
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Chaki, Sankar P., Rola Barhoumi, and Gonzalo M. Rivera. "Actin remodeling by Nck regulates endothelial lumen formation." Molecular Biology of the Cell 26, no. 17 (September 2015): 3047–60. http://dx.doi.org/10.1091/mbc.e15-06-0338.

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Multiple angiogenic cues modulate phosphotyrosine signaling to promote vasculogenesis and angiogenesis. Despite its functional and clinical importance, how vascular cells integrate phosphotyrosine-dependent signaling to elicit cytoskeletal changes required for endothelial morphogenesis remains poorly understood. The family of Nck adaptors couples phosphotyrosine signals with actin dynamics and therefore is well positioned to orchestrate cellular processes required in vascular formation and remodeling. Culture of endothelial cells in three-dimensional collagen matrices in the presence of VEGF stimulation was combined with molecular genetics, optical imaging, and biochemistry to show that Nck-dependent actin remodeling promotes endothelial cell elongation and proper organization of VE-cadherin intercellular junctions. Major morphogenetic defects caused by abrogation of Nck signaling included loss of endothelial apical-basal polarity and impaired lumenization. Time-lapse imaging using a Förster resonance energy transfer biosensor, immunostaining with phospho-specific antibodies, and GST pull-down assays showed that Nck determines spatiotemporal patterns of Cdc42/aPKC activation during endothelial morphogenesis. Our results demonstrate that Nck acts as an important hub integrating angiogenic cues with cytoskeletal changes that enable endothelial apical-basal polarization and lumen formation. These findings point to Nck as an emergent target for effective antiangiogenic therapy.
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Rodríguez-Fraticelli, Alejo E., Muriel Auzan, Miguel A. Alonso, Michel Bornens, and Fernando Martín-Belmonte. "Cell confinement controls centrosome positioning and lumen initiation during epithelial morphogenesis." Journal of Cell Biology 198, no. 6 (September 10, 2012): 1011–23. http://dx.doi.org/10.1083/jcb.201203075.

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Epithelial organ morphogenesis involves sequential acquisition of apicobasal polarity by epithelial cells and development of a functional lumen. In vivo, cells perceive signals from components of the extracellular matrix (ECM), such as laminin and collagens, as well as sense physical conditions, such as matrix stiffness and cell confinement. Alteration of the mechanical properties of the ECM has been shown to promote cell migration and invasion in cancer cells, but the effects on epithelial morphogenesis have not been characterized. We analyzed the effects of cell confinement on lumen morphogenesis using a novel, micropatterned, three-dimensional (3D) Madin-Darby canine kidney cell culture method. We show that cell confinement, by controlling cell spreading, limits peripheral actin contractility and promotes centrosome positioning and lumen initiation after the first cell division. In addition, peripheral actin contractility is mediated by master kinase Par-4/LKB1 via the RhoA–Rho kinase–myosin II pathway, and inhibition of this pathway restores lumen initiation in minimally confined cells. We conclude that cell confinement controls nuclear–centrosomal orientation and lumen initiation during 3D epithelial morphogenesis.
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Hirai, Yohei, Derek Radisky, Rosanne Boudreau, Marina Simian, Mary E. Stevens, Yumiko Oka, Kyoko Takebe, Shinichiro Niwa, and Mina J. Bissell. "Epimorphin Mediates Mammary Luminal Morphogenesis through Control of C/EBPβ." Journal of Cell Biology 153, no. 4 (May 14, 2001): 785–94. http://dx.doi.org/10.1083/jcb.153.4.785.

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We have shown previously that epimorphin (EPM), a protein expressed on the surface of myoepithelial and fibroblast cells of the mammary gland, acts as a multifunctional morphogen of mammary epithelial cells. Here, we present the molecular mechanism by which EPM mediates luminal morphogenesis. Treatment of cells with EPM to induce lumen formation greatly increases the overall expression of transcription factor CCAAT/enhancer binding protein (C/EBP)β and alters the relative expression of its two principal isoforms, LIP and LAP. These alterations were shown to be essential for the morphogenetic activities, since constitutive expression of LIP was sufficient to produce lumen formation, whereas constitutive expression of LAP blocked EPM-mediated luminal morphogenesis. Furthermore, in a transgenic mouse model in which EPM expression was expressed in an apolar fashion on the surface of mammary epithelial cells, we found increased expression of C/EBPβ, increased relative expression of LIP to LAP, and enlarged ductal lumina. Together, our studies demonstrate a role for EPM in luminal morphogenesis through control of C/EBPβ expression.
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Jung, Jae-Joon, Shivangi M. Inamdar, Ajit Tiwari, Ding Ye, Fang Lin, and Amit Choudhury. "Syntaxin 16 Regulates Lumen Formation during Epithelial Morphogenesis." PLoS ONE 8, no. 4 (April 23, 2013): e61857. http://dx.doi.org/10.1371/journal.pone.0061857.

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Montesano, R. "Retinoids induce lumen morphogenesis in mammary epithelial cells." Journal of Cell Science 115, no. 23 (December 1, 2002): 4419–31. http://dx.doi.org/10.1242/jcs.00164.

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Rodriguez-Fraticelli, Alejo E., Silvia Vergarajauregui, Dennis J. Eastburn, Anirban Datta, Miguel A. Alonso, Keith Mostov, and Fernando Martín-Belmonte. "The Cdc42 GEF Intersectin 2 controls mitotic spindle orientation to form the lumen during epithelial morphogenesis." Journal of Cell Biology 189, no. 4 (May 17, 2010): 725–38. http://dx.doi.org/10.1083/jcb.201002047.

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Epithelial organs are made of tubes and cavities lined by a monolayer of polarized cells that enclose the central lumen. Lumen formation is a crucial step in the formation of epithelial organs. The Rho guanosine triphosphatase (GTPase) Cdc42, which is a master regulator of cell polarity, regulates the formation of the central lumen in epithelial morphogenesis. However, how Cdc42 is regulated during this process is still poorly understood. Guanine nucleotide exchange factors (GEFs) control the activation of small GTPases. Using the three-dimensional Madin–Darby canine kidney model, we have identified a Cdc42-specific GEF, Intersectin 2 (ITSN2), which localizes to the centrosomes and regulates Cdc42 activation during epithelial morphogenesis. Silencing of either Cdc42 or ITSN2 disrupts the correct orientation of the mitotic spindle and normal lumen formation, suggesting a direct relationship between these processes. Furthermore, we demonstrated this direct relationship using LGN, a component of the machinery for mitotic spindle positioning, whose disruption also results in lumen formation defects.
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Willenborg, Carly, Jian Jing, Christine Wu, Hugo Matern, Jerome Schaack, Jemima Burden, and Rytis Prekeris. "Interaction between FIP5 and SNX18 regulates epithelial lumen formation." Journal of Cell Biology 195, no. 1 (October 3, 2011): 71–86. http://dx.doi.org/10.1083/jcb.201011112.

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During the morphogenesis of the epithelial lumen, apical proteins are thought to be transported via endocytic compartments to the site of the forming lumen, although the machinery mediating this transport remains to be elucidated. Rab11 GTPase and its binding protein, FIP5, are important regulators of polarized endocytic transport. In this study, we identify sorting nexin 18 as a novel FIP5-interacting protein and characterize the role of FIP5 and SNX18 in epithelial lumen morphogenesis. We show that FIP5 mediates the transport of apical proteins from apical endosomes to the apical plasma membrane and, along with SNX18, is required for the early stages of apical lumen formation. Furthermore, both proteins bind lipids, and FIP5 promotes the capacity of SNX18 to tubulate membranes, which implies a role for FIP5 and SNX18 in endocytic carrier formation and/or scission. In summary, the present findings support the hypothesis that this FIP5-SNX18 complex plays a pivotal role in the polarized transport of apical proteins during apical lumen initiation in epithelial cells.
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Dissertations / Theses on the topic "Lumen Morphogenesis"

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SYED, ABRAR HUSSAIN RIZVI. "ROLE OF IRSP53 IN EPITHELIAL POLARITY ESTABLISHMENT AND LUMEN MORPHOGENESIS." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/609620.

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Polarity establishment is essential for the normal development and morphogenesis of virtually all epithelial tissues. Loss of epithelial polarity has been implicated in many disorders including tumorigenesis and metastasis. Epithelial polarity is established by a multifaceted signalling cross-talk between a network of polarity determinants that include cell adhesion molecules, trafficking machinery, polarity complexes and the spindle orientation apparatus. Despite tremendous advance in defining the molecular details of how these processes are controlled, much remains to be understood as to how the coordination between all these components is achieved. IRSp53, a versatile molecule operating at the membrane-actin interface, has been reported to be involved in the process of epithelial polarity but the mechanisms through which it operates has, however, remained completely elusive. Here, we studied the processes through which IRSp53 plays a role in the establishment of epithelial polarity and lumen morphogenesis in MDCK and Caco-2 derived 3-D cysts. We further extended the relevance of our in vitro findings to the kidney morphogenesis in our genetically modified animal models. We found that IRSP53 is apically restricted at the luminal side of various epithelial tubular and glandular human, murine and zebrafish tissues. Further, IRSp53 is early recruited after the first cell division along the AMIS and essential for the formation of a single apical domain and the localized recruitment of aPKC and Podocalyxin (PDX). Molecularly, IRSp53 exerts this function by binding directly through a positively charged patch on its I-BAR-domain to the inactive form of RAB35, which co-localizes with IRSp53 at the onset of AMIS, and by controlling PDX trafficking. Additionally, membrane- and SH3- mediated interactions are required for proper localization and, thus, for the function of IRSp53. IRSp53 is also found to localize to the spindle poles and to aid in the proper orientation of the mitotic spindle during cystogenesis. Consistently, IRSp53 depletion causes spindle misorientation, leading to aberrant cell divisions and multi-lumen phenotype during epithelial cystogenesis. The critical physiological role of IRSp53 in epithelial morphogenesis is corroborated by the finding that genetic deletion of IRSp53 results in abnormal renal tubulogenesis, with profound defects in tubular polarity, architectural organization and lumen formation during both kidney development and in the adult kidneys either in IRSp53 zebrafish mutant lines and in IRSp53 KO murine models. We propose that the proper localisation of IRSp53 is pivotal for the assembly of macromolecular complexes on the apical domain of tubular and glandular epithelia which is, in turn, necessary for the proper kidney development by regulating cell polarity and lumen morphogenesis.
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Scarborough, Julie. "Morphogenesis in Drosophila melanogaster : an in vitro analysis." Thesis, St Andrews, 2007. http://hdl.handle.net/10023/337.

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Veligodskiy, Alexey. "The mechanisms of epithelial morphogenesis and de novo lumen formation : a balance of cell division, cellular tension, and vectorial fluid transport /." Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17870.

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Book chapters on the topic "Lumen Morphogenesis"

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Arecchi, Fortunato Tito. "Fiat Lux Versus Fiat Lumen: Quantum Effects in Linguistic Operations." In Lecture Notes in Morphogenesis, 143–53. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29483-4_8.

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Kaufman, M. H. "Occlusion of the Lumen of the neural tube, and its role in the early morphogenesis of the brain." In Spina bifida - neural tube defects, edited by P. Gless, J. Lorber, and D. Voth, 29–46. Berlin, Boston: De Gruyter, 1986. http://dx.doi.org/10.1515/9783110850307-006.

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Conference papers on the topic "Lumen Morphogenesis"

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Treder, Jadwiga, Anna Borkowska, Waldemar Treder, and Krzysztof Klamkowski. "The effects of LEDs on growth and morphogenesis of vegetable seedlings cultivated in growth chambers." In 2016 IEEE Lighting Conference of the Visegrad Countries (Lumen V4). IEEE, 2016. http://dx.doi.org/10.1109/lumenv.2016.7745542.

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