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12. Paralemmin-1 is expressed in lymphatic endothelial cells and modulates cell migration, cell maturation and tumor lymphangiogenesis

Author

Albrecht, Imke, Bieri, Raphael, Leu, Angela, Granacher, Philipp, Hagmann, Jörg, Kilimann, Manfred, and Christofori, Gerhard

Abstract

The lymphatic system, the network of lymphatic vessels and lymphoid organs, maintains the body fluid balance and ensures the immunological surveillance of the body. In the adult organism, the de novo formation of lymphatic vessels is mainly observed in pathological conditions. In contrast to the molecular mechanisms governing the generation of the lymphatic vasculature during embryogenesis, the processes underlying pathological lymphangiogenesis are less well understood. A genome-wide screen comparing the transcriptome of tumor-derived lymphatic endothelial cells with that of blood vessel endothelial cells identified paralemmin-1 as a protein prominently expressed in lymphatic endothelial cells. Paralemmin-1 is a lipid-anchored membrane protein that in fibroblasts and neurons plays a role in the regulation of cell shape, plasma membrane dynamics and cell motility. Here, we show that paralemmin-1 is expressed in tumor-derived lymphatic endothelial cells as well as in lymphatic endothelial cells of normal, non-tumorigenic tissue. Paralemmin-1 represses cell migration and delays the formation of tube-like structures of lymphatic endothelial cells in vitro by modulating cell-substrate adhesion, filopodia formation and plasma membrane blebbing. While constitutive genetic ablation of paralemmin-1 expression in mice has no effect on the development and physiological function of the lymphatic system, the loss of paralemmin-1 impaired tumor-associated lymphangiogenesis. Together, these results newly identify paralemmin-1 as a protein highly expressed in lymphatic endothelial cells. Similar to its function in neurons, it may link the cytoskeleton to the plasma membrane and thereby modulate lymphatic endothelial cell adhesion, migration and lymphangiogenesis

Published
2018

13. Essential role for cholesterol in the delivery of exogenous antigens to the MHC class I-presentation pathway

Author

Albrecht, Imke, Gatfield, John, Mini, Thierry, Jeno, Paul, Pieters, Jean, Albrecht, Imke, Gatfield, John, Mini, Thierry, Jeno, Paul, and Pieters, Jean

Abstract

Cross-presentation, which is crucial for the generation of immunity against virus-infected and tumor cells, requires exogenous antigens to be internalized into antigen-presenting cells (APCs) followed by translocation to the cytosol by unknown mechanisms. One important entry route for such antigens is macropinocytosis. We here describe that cholesterol is essential for cross-presentation of antigens loaded via macropinocytosis into APCs. Modification of antigens by palmitoylation to target antigens to cholesterol-enriched plasma membrane domains resulted in a dramatically increased T cell activation. These results define cholesterol as an essential factor for cross-presentation and suggest that specific modification of antigens to increase their affinity for cholesterol may be utilized to enhance immunity

Published
2017

15. Studies on the role of cholesterol and coronin 1 in antigen-presenting cells

Author

Albrecht, Imke, Pieters, Jean, and Rolink, Antonius G.

Abstract

Antigen recognition and presentation to subsequently induce an appropriate host response is dependent on the action of antigen-presenting cells such as dendritic cells and macrophages. In this thesis, the function of cholesterol and coroninin antigen-presenting cells was studied. In the first part of this thesis, the delivery of exogenous antigens into the MHC class I pathway, termed cross-presentation, was investigated. Cross-presentation is important for the establishment of an immune response against viruses or tumour cells in vivo. Antigens to be cross-presented are frequently internalized via macropinocytosis. Here it is shown, that by cholesterol-depletion of antigen-presenting cells macropinosome formation was abolished resulting in an impaired crosspresentation of exogenous antigens. In accordance with a role of cholesterol in cross-presentation, modification of antigens by palmitoylation, a modification known to increase the affinity to cholesterol, resulted in a strongly enhanced uptake and improved cross-presentation of the antigen. Together, these results indicate that cholesterol plays an important role in macropinocytosis and in the subsequent delivery of antigens into the MHC class I pathway. To explore palmitoylation as a modification that would enhance cross-presentation of antigens, we found that such modification often results in the insolubility of the modified antigen. For specific antigens however the use of palmitoylation to improve cross-presentation of soluble proteins could be explored for the development of new vaccines. The second part of this thesis focused on coronin 1, a member of the WD repeat protein family of actin-binding proteins termed coronins. In contrast to the other mammalian coronins, coroninis expressed predominantly in leukocytes arguing for a role in leukocyte specific processes. To understand a function for coronin 1, the structure of coroninwas analyzed. Coroninconsists of three structural domains: a N-terminal region containingWD40 repeats, which is connected by a linker region with a C-terminal coiled coil domain. Coroninoccurs in vivo as homotrimeric complexes, which associate with the plasma membrane and with the cytoskeleton via two distinct binding domains. It was found, that association of coroninwith the cytoskeleton was mediated by coiled coil induced trimerization of a stretch of positively charged residues within the linker region. In contrast, plasma membrane binding was independent of the oligomerization state of coroninand required the presence of the N-terminal, WD repeat-containing domain. By bridging the F-actin cytoskeleton with the plasma membrane coronin1 may serve as a linker integrating outside signals with the remodelling of the F-actin cytoskeleton.

Published
2005
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16. Further pharmacological and genetic evidence for the efficacy of PlGF inhibition in cancer and eye disease

Author

Van de Veire, Sara, Stalmans, Ingeborg, Heindryckx, Femke, Oura, Hajimu, Tijeras-Raballand, Annemilaï, Schmidt, Thomas, Loges, Sonja, Albrecht, Imke, Jonckx, Bart, Vinckier, Stefan, Van Steenkiste, Christophe, Tugues, Sònia, Rolny, Charlotte, De Mol, Maria, Dettori, Daniela, Hainaud, Patricia, Coenegrachts, Lieve, Contreres, Jean-Olivier, Van Bergen, Tine, Cuervo, Henar, Xiao, Wei-Hong, Le Henaff, Carole, Buysschaert, Ian, Kharabi Masouleh, Behzad, Geerts, Anja, Schomber, Tibor, Bonnin, Philippe, Lambert, Vincent, Haustraete, Jurgen, Zacchigna, Serena, Rakic, Jean-Marie, Jiménez, Wladimiro, Noël, Agnes, Giacca, Mauro, Colle, Isabelle, Foidart, Jean-Michel, Tobelem, Gerard, Morales-Ruiz, Manuel, Vilar, José, Maxwell, Patrick, Vinores, Stanley A., Carmeliet, Geert, Dewerchin, Mieke, Claesson-Welsh, Lena, Dupuy, Evelyne, Van Vlierberghe, Hans, Christofori, Gerhard, Mazzone, Massimiliano, Detmar, Michael, Collen, Désiré, Carmeliet, Peter, Van de Veire, Sara, Stalmans, Ingeborg, Heindryckx, Femke, Oura, Hajimu, Tijeras-Raballand, Annemilaï, Schmidt, Thomas, Loges, Sonja, Albrecht, Imke, Jonckx, Bart, Vinckier, Stefan, Van Steenkiste, Christophe, Tugues, Sònia, Rolny, Charlotte, De Mol, Maria, Dettori, Daniela, Hainaud, Patricia, Coenegrachts, Lieve, Contreres, Jean-Olivier, Van Bergen, Tine, Cuervo, Henar, Xiao, Wei-Hong, Le Henaff, Carole, Buysschaert, Ian, Kharabi Masouleh, Behzad, Geerts, Anja, Schomber, Tibor, Bonnin, Philippe, Lambert, Vincent, Haustraete, Jurgen, Zacchigna, Serena, Rakic, Jean-Marie, Jiménez, Wladimiro, Noël, Agnes, Giacca, Mauro, Colle, Isabelle, Foidart, Jean-Michel, Tobelem, Gerard, Morales-Ruiz, Manuel, Vilar, José, Maxwell, Patrick, Vinores, Stanley A., Carmeliet, Geert, Dewerchin, Mieke, Claesson-Welsh, Lena, Dupuy, Evelyne, Van Vlierberghe, Hans, Christofori, Gerhard, Mazzone, Massimiliano, Detmar, Michael, Collen, Désiré, and Carmeliet, Peter

Abstract

Our findings that PlGF is a cancer target and anti-PlGF is useful for anticancer treatment have been challenged by Bais et al. Here we take advantage of carcinogen-induced and transgenic tumor models as well as ocular neovascularization to report further evidence in support of our original findings of PlGF as a promising target for anticancer therapies. We present evidence for the efficacy of additional anti-PlGF antibodies and their ability to phenocopy genetic deficiency or silencing of PlGF in cancer and ocular disease but also show that not all anti-PlGF antibodies are effective. We also provide additional evidence for the specificity of our anti-PlGF antibody and experiments to suggest that anti-PlGF treatment will not be effective for all tumors and why. Further, we show that PlGF blockage inhibits vessel abnormalization rather than density in certain tumors while enhancing VEGF-targeted inhibition in ocular disease. Our findings warrant further testing of anti-PlGF therapies.

Published
2010
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17. Suppressive Effects of Vascular Endothelial Growth Factor-B on Tumor Growth in a Mouse Model of Pancreatic Neuroendocrine Tumorigenesis

Author

University of Helsinki, Research Programs Unit, Albrecht, Imke, Kopfstein, Lucie, Strittmatter, Karin, Schomber, Tibor, Falkevall, Annelie, Hagberg, Carolina E., Lorentz, Pascal, Jeltsch, Michael, Alitalo, Kari, Eriksson, Ulf, Christofori, Gerhard, Pietras, Kristian, University of Helsinki, Research Programs Unit, Albrecht, Imke, Kopfstein, Lucie, Strittmatter, Karin, Schomber, Tibor, Falkevall, Annelie, Hagberg, Carolina E., Lorentz, Pascal, Jeltsch, Michael, Alitalo, Kari, Eriksson, Ulf, Christofori, Gerhard, and Pietras, Kristian

Published
2010

20. Suppressive Effects of Vascular Endothelial Growth Factor-B on Tumor Growth in a Mouse Model of Pancreatic Neuroendocrine Tumorigenesis

Author

Albrecht, Imke, primary, Kopfstein, Lucie, additional, Strittmatter, Karin, additional, Schomber, Tibor, additional, Falkevall, Annelie, additional, Hagberg, Carolina E., additional, Lorentz, Pascal, additional, Jeltsch, Michael, additional, Alitalo, Kari, additional, Eriksson, Ulf, additional, Christofori, Gerhard, additional, and Pietras, Kristian, additional

Published
2010
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21. Abstract LB-362: PlGF inhibition phenocopies PlGF deficiency in cancer

Author

Schmidt, Thomas, primary, Van de Veire, Sara, additional, Heindryckx, Femke, additional, Oura, Hajimu, additional, Tijeras-Raballand, Annemilaï, additional, Loges, Sonja, additional, Albrecht, Imke, additional, Jonckx, Bart, additional, Vinckier, Stefan, additional, Van Steenkiste, Christophe, additional, Tugues, Sònia, additional, Rolny, Charlotte, additional, De Mol, Maria, additional, Dettori, Daniela, additional, Hainaud, Patricia, additional, Coenegrachts, Lieve, additional, Contreres, Jean-Olivier, additional, Cuervo, Henar, additional, Henaff, Carole Le, additional, Buysschaert, Ian, additional, Masouleh, Behzad Kharabi, additional, Geerts, Anja, additional, Schomber, Tibor, additional, Bonnin, Philippe, additional, Haustraete, Juergen, additional, Zacchigna, Serena, additional, Jiménez, Wladimiro, additional, Giacca, Mauro, additional, Colle, Isabelle, additional, Tobelem, Gerard, additional, Morales-Ruiz, Manuel, additional, Vilar, José, additional, Carmeliet, Geert, additional, Dewerchin, Mieke, additional, Claesson-Welsh, Lena, additional, Dupuy, Evelyne, additional, Van Vlierberghe, Hans, additional, Christofori, Gerhard, additional, Mazzone, Massimiliano, additional, Detmar, Michael, additional, Collen, Désiré, additional, and Carmeliet, Peter, additional

Published
2010
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22. Further Pharmacological and Genetic Evidence for the Efficacy of PlGF Inhibition in Cancer and Eye Disease

Author

Van de Veire, Sara, primary, Stalmans, Ingeborg, additional, Heindryckx, Femke, additional, Oura, Hajimu, additional, Tijeras-Raballand, Annemilaï, additional, Schmidt, Thomas, additional, Loges, Sonja, additional, Albrecht, Imke, additional, Jonckx, Bart, additional, Vinckier, Stefan, additional, Van Steenkiste, Christophe, additional, Tugues, Sònia, additional, Rolny, Charlotte, additional, De Mol, Maria, additional, Dettori, Daniela, additional, Hainaud, Patricia, additional, Coenegrachts, Lieve, additional, Contreres, Jean-Olivier, additional, Van Bergen, Tine, additional, Cuervo, Henar, additional, Xiao, Wei-Hong, additional, Le Henaff, Carole, additional, Buysschaert, Ian, additional, Masouleh, Behzad Kharabi, additional, Geerts, Anja, additional, Schomber, Tibor, additional, Bonnin, Philippe, additional, Lambert, Vincent, additional, Haustraete, Jurgen, additional, Zacchigna, Serena, additional, Rakic, Jean-Marie, additional, Jiménez, Wladimiro, additional, Noël, Agnes, additional, Giacca, Mauro, additional, Colle, Isabelle, additional, Foidart, Jean-Michel, additional, Tobelem, Gerard, additional, Morales-Ruiz, Manuel, additional, Vilar, José, additional, Maxwell, Patrick, additional, Vinores, Stanley A., additional, Carmeliet, Geert, additional, Dewerchin, Mieke, additional, Claesson-Welsh, Lena, additional, Dupuy, Evelyne, additional, Van Vlierberghe, Hans, additional, Christofori, Gerhard, additional, Mazzone, Massimiliano, additional, Detmar, Michael, additional, Collen, Désiré, additional, and Carmeliet, Peter, additional

Published
2010
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23. Regulation of T cell survival through coronin-1–mediated generation of inositol-1,4,5-trisphosphate and calcium mobilization after T cell receptor triggering

Author

Mueller, Philipp, primary, Massner, Jan, additional, Jayachandran, Rajesh, additional, Combaluzier, Benoit, additional, Albrecht, Imke, additional, Gatfield, John, additional, Blum, Carmen, additional, Ceredig, Rod, additional, Rodewald, Hans-Reimer, additional, Rolink, Antonius G, additional, and Pieters, Jean, additional

Published
2008
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29. Paralemmin-1 is expressed in lymphatic endothelial cells and modulates cell migration, cell maturation and tumor lymphangiogenesis

Author

Albrecht, Imke, Bieri, Raphael, Leu, Angela, Granacher, Philipp, Hagmann, Jörg, Kilimann, Manfred, Christofori, Gerhard, Albrecht, Imke, Bieri, Raphael, Leu, Angela, Granacher, Philipp, Hagmann, Jörg, Kilimann, Manfred, and Christofori, Gerhard

Abstract

The lymphatic system, the network of lymphatic vessels and lymphoid organs, maintains the body fluid balance and ensures the immunological surveillance of the body. In the adult organism, the de novo formation of lymphatic vessels is mainly observed in pathological conditions. In contrast to the molecular mechanisms governing the generation of the lymphatic vasculature during embryogenesis, the processes underlying pathological lymphangiogenesis are less well understood. A genome-wide screen comparing the transcriptome of tumor-derived lymphatic endothelial cells with that of blood vessel endothelial cells identified paralemmin-1 as a protein prominently expressed in lymphatic endothelial cells. Paralemmin-1 is a lipid-anchored membrane protein that in fibroblasts and neurons plays a role in the regulation of cell shape, plasma membrane dynamics and cell motility. Here, we show that paralemmin-1 is expressed in tumor-derived lymphatic endothelial cells as well as in lymphatic endothelial cells of normal, non-tumorigenic tissue. Paralemmin-1 represses cell migration and delays the formation of tube-like structures of lymphatic endothelial cells in vitro by modulating cell-substrate adhesion, filopodia formation and plasma membrane blebbing. While constitutive genetic ablation of paralemmin-1 expression in mice has no effect on the development and physiological function of the lymphatic system, the loss of paralemmin-1 impaired tumor-associated lymphangiogenesis. Together, these results newly identify paralemmin-1 as a protein highly expressed in lymphatic endothelial cells. Similar to its function in neurons, it may link the cytoskeleton to the plasma membrane and thereby modulate lymphatic endothelial cell adhesion, migration and lymphangiogenesis

30. Essential role for cholesterol in the delivery of exogenous antigens to the MHC class I-presentation pathway

Author

Albrecht, Imke, Gatfield, John, Mini, Thierry, Jeno, Paul, Pieters, Jean, Albrecht, Imke, Gatfield, John, Mini, Thierry, Jeno, Paul, and Pieters, Jean

Abstract

Cross-presentation, which is crucial for the generation of immunity against virus-infected and tumor cells, requires exogenous antigens to be internalized into antigen-presenting cells (APCs) followed by translocation to the cytosol by unknown mechanisms. One important entry route for such antigens is macropinocytosis. We here describe that cholesterol is essential for cross-presentation of antigens loaded via macropinocytosis into APCs. Modification of antigens by palmitoylation to target antigens to cholesterol-enriched plasma membrane domains resulted in a dramatically increased T cell activation. These results define cholesterol as an essential factor for cross-presentation and suggest that specific modification of antigens to increase their affinity for cholesterol may be utilized to enhance immunity

31. Placental growth factor-1 attenuates vascular endothelial growth factor-A-dependent tumor angiogenesis during beta cell carcinogenesis.

Author

Schomber T, Kopfstein L, Djonov V, Albrecht I, Baeriswyl V, Strittmatter K, and Christofori G

Subjects
Animals, Collagen chemistry, Dimerization, Enzyme-Linked Immunosorbent Assay, Humans, Islets of Langerhans metabolism, Methylmethacrylate chemistry, Mice, Mice, Transgenic, Neoplasm Invasiveness, Pancreatic Neoplasms metabolism, Placenta Growth Factor, Pregnancy Proteins metabolism, Insulin-Secreting Cells metabolism, Neovascularization, Pathologic, Pancreatic Neoplasms pathology, Pregnancy Proteins physiology, Vascular Endothelial Growth Factor A metabolism
Abstract

Members of the vascular endothelial growth factor (VEGF) family are critical players in angiogenesis and lymphangiogenesis. Although VEGF-A has been shown to exert fundamental functions in physiologic and pathologic angiogenesis, the exact role of the VEGF family member placental growth factor (PlGF) in tumor angiogenesis has remained controversial. To gain insight into PlGF function during tumor angiogenesis, we have generated transgenic mouse lines expressing human PlGF-1 in the beta cells of the pancreatic islets of Langerhans (Rip1PlGF-1). In single-transgenic Rip1PlGF-1 mice, intra-insular blood vessels are found highly dilated, whereas islet physiology is unaffected. Upon crossing of these mice with the Rip1Tag2 transgenic mouse model of pancreatic beta cell carcinogenesis, tumors of double-transgenic Rip1Tag2;Rip1PlGF-1 mice display reduced growth due to attenuated tumor angiogenesis. The coexpression of transgenic PlGF-1 and endogenous VEGF-A in the beta tumor cells of double-transgenic animals causes the formation of low-angiogenic hPlGF-1/mVEGF-A heterodimers at the expense of highly angiogenic mVEGF-A homodimers resulting in diminished tumor angiogenesis and reduced tumor infiltration by neutrophils, known to contribute to the angiogenic switch in Rip1Tag2 mice. The results indicate that the ratio between the expression levels of two members of the VEGF family of angiogenic factors, PlGF-1 and VEGF-A, determines the overall angiogenic activity and, thus, the extent of tumor angiogenesis and tumor growth.

Published
2007
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