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6. Annexin A1 Tethers Membrane Contact Sites that Mediate ER to Endosome Cholesterol Transport

Author

Eden, Emily R., Sanchez-Heras, Elena, Tsapara, Anna, Sobota, Andrzej, Levine, Tim P., and Futter, Clare E.

Subjects
Developmental Biology
Abstract

SummaryMembrane contact sites between the ER and multivesicular endosomes/bodies (MVBs) play important roles in endosome positioning and fission and in neurite outgrowth. ER-MVB contacts additionally function in epidermal growth factor receptor (EGFR) tyrosine kinase downregulation by providing sites where the ER-localized phosphatase, PTP1B, interacts with endocytosed EGFR before the receptor is sorted onto intraluminal vesicles (ILVs). Here we show that these contacts are tethered by annexin A1 and its Ca2+-dependent ligand, S100A11, and form a subpopulation of differentially regulated contact sites between the ER and endocytic organelles. Annexin A1-regulated contacts function in the transfer of ER-derived cholesterol to the MVB when low-density lipoprotein-cholesterol in endosomes is low. This sterol traffic depends on interaction between ER-localized VAP and endosomal oxysterol-binding protein ORP1L, and is required for the formation of ILVs within the MVB and thus for the spatial regulation of EGFR signaling.

Published
2016
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10. Istaroxime Inhibits Motility and Down-Regulates Orai1 Expression, SOCE and FAK Phosphorylation in Prostate Cancer Cells

Author

Stagno, Matias Julian, primary, Zacharopoulou, Nefeli, additional, Bochem, Jonas, additional, Tsapara, Anna, additional, Pelzl, Lisann, additional, al-Maghout, Tamer, additional, Kallergi, Galatea, additional, Alkahtani, Saad, additional, Alevizopoulos, Konstantinos, additional, Dimas, Konstantinos, additional, Calogeropoulou, Theodora, additional, Warmann, Steven W., additional, Lang, Florian, additional, Schmid, Evi, additional, and Stournaras, Christos, additional

Published
2017
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11. Functional characterization and anti-cancer action of the clinical phase II cardiac Na+/K+ ATPase inhibitor istaroxime: in vitro and in vivo properties and cross talk with the membrane androgen receptor

Author

Alevizopoulos, Konstantinos, primary, Dimas, Konstantinos, additional, Papadopoulou, Natalia, additional, Schmidt, Eva-Maria, additional, Tsapara, Anna, additional, Alkahtani, Saad, additional, Honisch, Sabina, additional, Prousis, Kyriakos C., additional, Alarifi, Saud, additional, Calogeropoulou, Theodora, additional, Lang, Florian, additional, and Stournaras, Christos, additional

Published
2016
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12. Chorein addiction in VPS13A overexpressing rhabdomyosarcoma cells

Author

Honisch, Sabina, primary, Yu, Willi, additional, Liu, Guilai, additional, Alesutan, Ioana, additional, Towhid, Syeda T., additional, Tsapara, Anna, additional, Schleicher, Sabine, additional, Handgretinger, Rupert, additional, Stournaras, Christos, additional, and Lang, Florian, additional

Published
2015
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13. Chorein Sensitive Arrangement of Cytoskeletal Architecture

Author

Honisch, Sabina, primary, Gu, Shuchen, additional, vom Hagen, Jennifer Müller, additional, Alkahtani, Saad, additional, Al Kahtane, Abdullah A., additional, Tsapara, Anna, additional, Hermann, Andreas, additional, Storch, Alexander, additional, Schöls, Ludger, additional, Lang, Florian, additional, and Stournaras, Christos, additional

Published
2015
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21. Tight Junctions and the Regulation of Epithelial Cell Proliferation and Gene Expression.

Author

Gonzalez-Mariscal, Lorenza, Kavanagh, Emma, Tsapara, Anna, Matter, Karl, and Balda, Maria S.

Abstract

Cell interactions with the extracellular matrix and neighboring cells regulate epithelial cell proliferation and differentiation. Tight Junctions are the most apical cell-cell junctions of epithelial cells and evidence indicates that they participate in the suppression of cell proliferation and stimulation of differentiation. Some tight junction components are expressed at increased levels in differentiated versus proliferating cells; and their down-regulation has been linked to epithelial-mesenchymal transition as well as cancer. Other tight junction proteins are also found in the nucleus of proliferating cells and have been linked to the regulation of cell proliferation, transcription and RNA processing. Therefore, it seems that the accumulation of proteins at forming tight junctions is related to signaling pathways that control cell growth arrest and differentiation. We propose a model in which the assembly state of tight junctions is used as a sensor for cell proliferation and density. When cell density increases, the expression levels of tight junction proteins that are inhibitors of proliferation increase and they become stabilized at the forming junctions, resulting in the suppression of proliferation promoting signaling pathways. Furthermore, the tight junction signaling pathways in connection with signals from other cell-cell and extracellular matrix interactions ensure that epithelial cells stop to proliferate and begin to differentiate. [ABSTRACT FROM AUTHOR]

Published
2006
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25. The RhoA activator GEF-H1/Lfc is a transforming growth factor-beta target gene and effector that regulates alpha-smooth muscle actin expression and cell migration.

Author

Tsapara A, Luthert P, Greenwood J, Hill CS, Matter K, and Balda MS

Subjects
Actins genetics, Animals, Cell Adhesion physiology, Cell Differentiation physiology, Cells, Cultured, Gene Expression Regulation, Guanine Nucleotide Exchange Factors genetics, Humans, Microarray Analysis, Retinal Pigment Epithelium cytology, Retinal Pigment Epithelium physiology, Rho Guanine Nucleotide Exchange Factors, Signal Transduction physiology, Smad4 Protein metabolism, Swine, rhoA GTP-Binding Protein genetics, Actins metabolism, Cell Movement physiology, Guanine Nucleotide Exchange Factors metabolism, Transforming Growth Factor beta metabolism, rhoA GTP-Binding Protein metabolism
Abstract

Maintenance of the epithelial phenotype is crucial for tissue homeostasis. In the retina, dedifferentiation and loss of integrity of the retinal pigment epithelium (RPE) leads to retinal dysfunction and fibrosis. Transforming growth factor (TGF)-beta critically contributes to RPE dedifferentiation and induces various responses, including increased Rho signaling, up-regulation of alpha-smooth muscle actin (SMA), and cell migration and dedifferentiation. Cellular TGF-beta responses are stimulated by different signal transduction pathways: some are Smad dependent and others Smad independent. Alterations in Rho signaling are crucial to both types of TGF-beta signaling, but how TGF-beta-stimulates Rho signaling is poorly understood. Here, we show that primary RPE cells up-regulated GEF-H1 in response to TGF-beta. GEF-H1 was the only detectable Rho exchange factor increased by TGF-beta1 in a genome-wide expression analysis. GEF-H1 induction was Smad4-dependant and led to Rho activation. GEF-H1 inhibition counteracted alpha-SMA up-regulation and cell migration. In patients with retinal detachments and fibrosis, migratory RPE cells exhibited increased GEF-H1 expression, indicating that induction occurs in diseased RPE in vivo. Our data indicate that GEF-H1 is a target and functional effector of TGF-beta by orchestrating Rho signaling to regulate gene expression and cell migration, suggesting that it represents a new marker and possible therapeutic target for degenerative and fibrotic diseases.

Published
2010
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