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2. HIF-1α regulates the interaction of chronic lymphocytic leukemia cells with the tumor microenvironment

Author

Valsecchi, Roberta, Coltella, Nadia, Belloni, Daniela, Ponente, Manfredi, ten Hacken, Elisa, Scielzo, Cristina, Scarfò, Lydia, Bertilaccio, Maria Teresa Sabrina, Brambilla, Paola, Lenti, Elisa, Martinelli Boneschi, Filippo, Brendolan, Andrea, Ferrero, Elisabetta, Ferrarini, Marina, Ghia, Paolo, Tonon, Giovanni, Ponzoni, Maurilio, Caligaris-Cappio, Federico, and Bernardi, Rosa

Published
2016
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3. Transcription factor TLX1 controls retinoic acid signaling to ensure spleen development

Author

Lenti, Elisa, Farinello, Diego, Yokoyama, Kazunari K., Penkov, Dmitry, Castagnaro, Laura, Lavorgna, Giovanni, Wuputra, Kenly, Sandell, Lisa L., Tjaden, Naomi E. Butler, Bernassola, Francesca, Caridi, Nicoletta, De Antoni, Anna, Wagner, Michael, Kozinc, Katja, Niederreither, Karen, Blasi, Francesco, Pasini, Diego, Majdic, Gregor, Tonon, Giovanni, Trainor, Paul A., and Brendolan, Andrea

Subjects
Tretinoin -- Genetic aspects -- Physiological aspects -- Research, Splenic diseases -- Genetic aspects -- Causes of -- Research, Transcription factors -- Analysis, Health care industry
Abstract

The molecular mechanisms that underlie spleen development and congenital asplenia, a condition linked to increased risk of overwhelming infections, remain largely unknown. The transcription factor TLX1 controls cell fate specification and organ expansion during spleen development, and Tlx1 deletion causes asplenia in mice. Deregulation of TLX1 expression has recently been proposed in the pathogenesis of congenital asplenia in patients carrying mutations of the gene-encoding transcription factor SF-1. Herein, we have shown that TLX1-dependent regulation of retinoic acid (RA) metabolism is critical for spleen organogenesis. In a murine model, loss of Tlx1 during formation of the splenic anlage increased RA signaling by regulating several genes involved in RA metabolism. Uncontrolled RA activity resulted in premature differentiation of mesenchymal cells and reduced vasculogenesis of the splenic primordium. Pharmacological inhibition of RA signaling in Tlx1- deficient animals partially rescued the spleen defect. Finally, spleen growth was impaired in mice lacking either cytochrome P450 26B1 (Cyp26b1), which results in excess RA, or retinol dehydrogenase 10 (Rdh10), which results in RA deficiency. Together, these findings establish TLX1 as a critical regulator of RA metabolism and provide mechanistic insights into the molecular determinants of human congenital asplenia., Introduction The mammalian spleen is a secondary lymphoid organ that plays a central role in host defense. As a result, asplenia or hyposplenia and postsplenectomy patients often have an increased [...]

Published
2016
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5. Fate mapping and scRNA sequencing reveal origin and diversity of lymph node stromal precursors

Author

Lenti, Elisa, primary, Genovese, Luca, additional, Bianchessi, Silvia, additional, Maurizio, Aurora, additional, Sain, Simona Baghai, additional, di Lillo, Alessia, additional, Mattavelli, Greta, additional, Harel, Itamar, additional, Bernassola, Francesca, additional, Hehlgans, Thomas, additional, Pfeffer, Klaus, additional, Crosti, Mariacristina, additional, Abrignani, Sergio, additional, Evans, Sylvia M., additional, Sitia, Giovanni, additional, Guimarães-Camboa, Nuno, additional, Russo, Vincenzo, additional, van de Pavert, Serge A., additional, Garcia-Manteiga, Jose Manuel, additional, and Brendolan, Andrea, additional

Published
2022
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8. Therapeutic Regeneration of Lymphatic and Immune Cell Functions upon Lympho-organoid Transplantation

Author

Lenti, Elisa, primary, Bianchessi, Silvia, additional, Proulx, Steven T., additional, Palano, Maria Teresa, additional, Genovese, Luca, additional, Raccosta, Laura, additional, Spinelli, Antonello, additional, Drago, Denise, additional, Andolfo, Annapaola, additional, Alfano, Massimo, additional, Petrova, Tatiana V., additional, Mukenge, Sylvain, additional, Russo, Vincenzo, additional, and Brendolan, Andrea, additional

Published
2019
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9. A retinoic acid-dependent stroma-leukemia crosstalk promotes chronic lymphocytic leukemia progression

Author

Farinello, Diego, primary, Wozińska, Monika, additional, Lenti, Elisa, additional, Genovese, Luca, additional, Bianchessi, Silvia, additional, Migliori, Edoardo, additional, Sacchetti, Nicolò, additional, di Lillo, Alessia, additional, Bertilaccio, Maria Teresa Sabrina, additional, de Lalla, Claudia, additional, Valsecchi, Roberta, additional, Gleave, Sabrina Bascones, additional, Lligé, David, additional, Scielzo, Cristina, additional, Mauri, Laura, additional, Ciampa, Maria Grazia, additional, Scarfò, Lydia, additional, Bernardi, Rosa, additional, Lazarevic, Dejan, additional, Gonzalez-Farre, Blanca, additional, Bongiovanni, Lucia, additional, Campo, Elias, additional, Cerutti, Andrea, additional, Ponzoni, Maurilio, additional, Pattini, Linda, additional, Caligaris-Cappio, Federico, additional, Ghia, Paolo, additional, and Brendolan, Andrea, additional

Published
2018
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13. Congenital Asplenia in Mice and Humans with Mutations in a Pbx/Nkx2-5/p15 Module

Author

Koss, Matthew, primary, Bolze, Alexandre, additional, Brendolan, Andrea, additional, Saggese, Matilde, additional, Capellini, Terence D., additional, Bojilova, Ekaterina, additional, Boisson, Bertrand, additional, Prall, Owen W.J., additional, Elliott, David A., additional, Solloway, Mark, additional, Lenti, Elisa, additional, Hidaka, Chisa, additional, Chang, Ching-Pin, additional, Mahlaoui, Nizar, additional, Harvey, Richard P., additional, Casanova, Jean-Laurent, additional, and Selleri, Licia, additional

Published
2012
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15. Nkx2-5+Islet1+ Mesenchymal Precursors Generate Distinct Spleen Stromal Cell Subsets and Participate in Restoring Stromal Network Integrity.

Author

Castagnaro, Laura, Lenti, Elisa, Maruzzelli, Sara, Spinardi, Laura, Migliori, Edoardo, Farinello, Diego, Sitia, Giovanni, Harrelson, Zachary, Evans, Sylvia?M., Guidotti, Luca?G., Harvey, Richard?P., and Brendolan, Andrea

Subjects
*MESENCHYMAL stem cells, *PROTEIN precursors, *STROMAL cells, *SPLEEN, *LYMPHOID tissue, *DENDRITIC cells
Abstract

Summary: Secondary lymphoid organ stromal cells comprise different subsets whose origins remain unknown. Herein, we exploit a genetic lineage-tracing approach to show that splenic fibroblastic reticular cells (FRCs), follicular dendritic cells (FDCs), marginal reticular cells (MRCs), and mural cells, but not endothelial cells, originate from embryonic mesenchymal progenitors of the Nkx2-5+Islet1+ lineage. This lineage include embryonic mesenchymal cells with lymphoid tissue organizer (LTo) activity capable also of supporting ectopic lymphoid-like structures and a subset of resident spleen stromal cells that proliferate and regenerate the splenic stromal microenvironment following resolution of a viral infection. These findings identify progenitor cells that generate stromal diversity in spleen development and repair and suggest the existence of multipotent stromal progenitors in the adult spleen with regenerative capacity. [ABSTRACT FROM AUTHOR]

Published
2013
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16. A retinoic acid-dependent stroma-leukemia crosstalk promotes chronic lymphocytic leukemia progression

Author

Luca Genovese, Andrea Cerutti, Maurilio Ponzoni, Cristina Scielzo, Sabrina Bascones Gleave, Claudia de Lalla, Edoardo Migliori, Linda Pattini, Lydia Scarfò, Laura Mauri, Dejan Lazarevic, Blanca Gonzalez-Farre, Elisa Lenti, Maria Grazia Ciampa, Paolo Ghia, Rosa Bernardi, Monika Wozińska, Nicolò Sacchetti, Diego Farinello, Lucia Bongiovanni, Federico Caligaris-Cappio, Elias Campo, Roberta Valsecchi, David Lligé, Maria Teresa Sabrina Bertilaccio, Silvia Bianchessi, Alessia di Lillo, Andrea Brendolan, Farinello, Diego, Wozińska, Monika, Lenti, Elisa, Genovese, Luca, Bianchessi, Silvia, Migliori, Edoardo, Sacchetti, Nicolò, Di Lillo, Alessia, Bertilaccio, Maria Teresa Sabrina, De Lalla, Claudia, Valsecchi, Roberta, Gleave, Sabrina Bascone, Lligé, David, Scielzo, Cristina, Mauri, Laura, Ciampa, Maria Grazia, Scarfò, Lydia, Bernardi, Rosa, Lazarevic, Dejan, Gonzalez-Farre, Blanca, Bongiovanni, Lucia, Campo, Elia, Cerutti, Andrea, Ponzoni, Maurilio, Pattini, Linda, Caligaris-Cappio, Federico, Ghia, Paolo, and Brendolan, Andrea

Subjects
0301 basic medicine, Male, Chemokine, Limfomes, Chronic lymphocytic leukemia, Retinoic acid, General Physics and Astronomy, chemistry.chemical_compound, Citoquines, Tumor Microenvironment, lcsh:Science, Coculture Technique, Multidisciplinary, biology, Chemistry (all), Gene Expression Regulation, Neoplastic, Leukemia, Chemokine secretion, Disease Progression, Cytokines, Female, Survival Analysi, Signal Transduction, Stromal cell, Science, Tretinoin, General Biochemistry, Genetics and Molecular Biology, Article, Cell Line, 03 medical and health sciences, Physics and Astronomy (all), Retinoids, medicine, Animals, Leucèmia limfocítica crònica, CXCL13, Tumor microenvironment, Retinoides, Biochemistry, Genetics and Molecular Biology (all), Animal, Stromal Cell, General Chemistry, medicine.disease, Chemokine CXCL13, Leukemia, Lymphocytic, Chronic, B-Cell, Survival Analysis, Coculture Techniques, Mice, Inbred C57BL, 030104 developmental biology, chemistry, biology.protein, Cancer research, lcsh:Q, Stromal Cells
Abstract

In chronic lymphocytic leukemia (CLL), the non-hematopoietic stromal microenvironment plays a critical role in promoting tumor cell recruitment, activation, survival, and expansion. However, the nature of the stromal cells and molecular pathways involved remain largely unknown. Here, we demonstrate that leukemic B lymphocytes induce the activation of retinoid acid synthesis and signaling in the microenvironment. Inhibition of RA-signaling in stromal cells causes deregulation of genes associated with adhesion, tissue organization and chemokine secretion including the B-cell chemokine CXCL13. Notably, reducing retinoic acid precursors from the diet or inhibiting RA-signaling through retinoid-antagonist therapy prolong survival by preventing dissemination of leukemia cells into lymphoid tissues. Furthermore, mouse and human leukemia cells could be distinguished from normal B-cells by their increased expression of Rarγ2 and RXRα, respectively. These findings establish a role for retinoids in murine CLL pathogenesis, and provide new therapeutic strategies to target the microenvironment and to control disease progression., The stromal microenvironment plays a key role in the expansion of chronic lymphocytic leukemia. Here, the authors use the Eµ-TCL1 mouse model to show that leukemic B-cells induce the activation of retinoic acid synthesis in stromal cells of the lymphoid microenvironment, and that impacting on retinoic acid signalling via diet or chemical inhibition prolonged survival by preventing leukemia dissemination and accumulation in lymphoid tissues.

Published
2018

17. HIF-1α regulates the interaction of chronic lymphocytic leukemia cells with the tumor microenvironment

Author

Maria Teresa Sabrina Bertilaccio, Federico Caligaris-Cappio, Manfredi Ponente, Paola Brambilla, Giovanni Tonon, Rosa Bernardi, Elisabetta Ferrero, Filippo Martinelli Boneschi, Paolo Ghia, Maurilio Ponzoni, Marina Ferrarini, Andrea Brendolan, Elisa Lenti, Elisa Ten Hacken, Lydia Scarfò, Cristina Scielzo, Daniela Belloni, Roberta Valsecchi, Nadia Coltella, Valsecchi, Roberta, Coltella, Nadia, Belloni, Daniela, Ponente, Manfredi, Ten Hacken, Elisa, Scielzo, Cristina, Scarfò, Lydia, Bertilaccio, Maria Teresa Sabrina, Brambilla, Paola, Lenti, Elisa, Boneschi, Filippo Martinelli, Brendolan, Andrea, Ferrero, Elisabetta, Ferrarini, Marina, Ghia, PAOLO PROSPERO, Tonon, Giovanni, Ponzoni, Maurilio, CALIGARIS CAPPIO, Federico, and Bernardi, Rosa

Subjects
0301 basic medicine, Stromal cell, Chronic lymphocytic leukemia, Immunology, Mice, Transgenic, Cell Communication, Biology, Biochemistry, 03 medical and health sciences, Chemokine receptor, Mice, 0302 clinical medicine, HEK293 Cell, immune system diseases, Bone Marrow, hemic and lymphatic diseases, medicine, Cell Adhesion, Tumor Microenvironment, Animals, Humans, Cell adhesion, neoplasms, Tumor microenvironment, Lymphoid Neoplasia, Cell adhesion molecule, Animal, Gene Expression Regulation, Leukemic, Stromal Cell, Hematology, Cell Biology, medicine.disease, Hypoxia-Inducible Factor 1, alpha Subunit, Leukemia, Lymphocytic, Chronic, B-Cell, Cell biology, Mice, Inbred C57BL, Leukemia, Chemotaxis, Leukocyte, 030104 developmental biology, medicine.anatomical_structure, HEK293 Cells, 030220 oncology & carcinogenesis, Bone marrow, Stromal Cells, Spleen, Human
Abstract

Hypoxia-inducible transcription factors (HIFs) regulate a wide array of adaptive responses to hypoxia and are often activated in solid tumors and hematologic malignancies due to intratumoral hypoxia and emerging new layers of regulation. We found that in chronic lymphocytic leukemia (CLL), HIF-1α is a novel regulator of the interaction of CLL cells with protective leukemia microenvironments and, in turn, is regulated by this interaction in a positive feedback loop that promotes leukemia survival and propagation. Through unbiased microarray analysis, we found that in CLL cells, HIF-1α regulates the expression of important chemokine receptors and cell adhesion molecules that control the interaction of leukemic cells with bone marrow and spleen microenvironments. Inactivation of HIF-1α impairs chemotaxis and cell adhesion to stroma, reduces bone marrow and spleen colonization in xenograft and allograft CLL mouse models, and prolongs survival in mice. Of interest, we found that in CLL cells, HIF-1α is transcriptionally regulated after coculture with stromal cells. Furthermore, HIF-1α messenger RNA levels vary significantly within CLL patients and correlate with the expression of HIF-1α target genes, including CXCR4, thus further emphasizing the relevance of HIF-1α expression to CLL pathogenesis.

Published
2016

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