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3. Epidermal growth factor receptor promotes glomerular injury and renal failure in rapidly progressive crescentic glomerulonephritis

Author

Bollee, Guillaume, Flamant, Martin, Schordan, Sandra, Fligny, Cecile, Rumpel, Elisabeth, Milon, Marine, Schordan, Eric, Sabaa, Nathalie, Vandermeersch, Sophie, Galaup, Ariane, Rodenas, Anita, Casal, Ibrahim, Sunnarborg, Susan W., Salant, David J., Kopp, Jeffrey B., Threadgill, David W., Quaggin, Susan E., Dussaule, Jean-Claude, Germain, Stephane, Mesnard, Laurent, Endlich, Karlhans, Boucheix, Claude, Belenfant, Xavier, Callard, Patrice, Endlich, Nicole, and Tharaux, Pierre-Louis

Subjects
Glomerulonephritis -- Risk factors -- Diagnosis -- Care and treatment -- Research, Biological sciences, Health
Abstract

Rapidly progressive glomerulonephritis (RPGN) is a life-threatening clinical syndrome and a morphological manifestation of severe glomerular injury that is marked by a proliferative histological pattern ('crescents') with accumulation of T cells and macrophages and proliferation of intrinsic glomerular cells. We show de novo induction of heparin-binding epidermal growth factor-like growth factor (HB-EGF) in intrinsic glomerular epithelial cells (podocytes) from both mice and humans with RPGN. HB-EGF induction increases phosphorylation of the epidermal growth factor receptor (EGFR, also known as ErbBl) in mice with RPGN. In HB-EGF-deficient mice, EGFR activation in glomeruli is absent and the course of RPGN is improved. Autocrine HB-EGF induces a phenotypic switch in podocytes in vitro. Conditional deletion of the Egfrgene from podocytes of mice alleviates the severity of RPGN. Likewise, pharmacological blockade of EGFR also improves the course of RPGN, even when started 4 d after the induction of experimental RPGN. This suggests that targeting the HB-EGF-EGFR pathway could also be beneficial in treatment of human RPGN., RPGN or crescentic glomerulonephritis is a life-threatening disease that destroys kidneys over a period of days to weeks. Proliferation of epithelial cells and infiltration of inflammatory cells lead to glomerular [...]

Published
2011
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4. Generation of Multipotent Early Lymphoid Progenitors from Human Embryonic Stem Cells

Author

Larbi, Aniya, primary, Mitjavila-Garcia, Maria Teresa, additional, Flamant, Stéphane, additional, Valogne, Yannick, additional, Clay, Denis, additional, Usunier, Benoît, additional, l'Homme, Bruno, additional, Féraud, Olivier, additional, Casal, Ibrahim, additional, Gobbo, Emilie, additional, Divers, Dominique, additional, Chapel, Alain, additional, Turhan, Ali G., additional, Bennaceur-Griscelli, Annelise, additional, and Haddad, Rima, additional

Published
2014
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6. Erratum: Epidermal growth factor receptor promotes glomerular injury and renal failure in rapidly progressive crescentic glomerulonephritis

Author

Bollée, Guillaume, primary, Flamant, Martin, additional, Schordan, Sandra, additional, Fligny, Cécile, additional, Rumpel, Elisabeth, additional, Milon, Marine, additional, Schordan, Eric, additional, Sabaa, Nathalie, additional, Vandermeersch, Sophie, additional, Galaup, Ariane, additional, Rodenas, Anita, additional, Casal, Ibrahim, additional, Sunnarborg, Susan W, additional, Salant, David J, additional, Kopp, Jeffrey B, additional, Threadgill, David W, additional, Quaggin, Susan E, additional, Dussaule, Jean-Claude, additional, Germain, Stéphane, additional, Mesnard, Laurent, additional, Endlich, Karlhans, additional, Boucheix, Claude, additional, Belenfant, Xavier, additional, Callard, Patrice, additional, Endlich, Nicole, additional, and Tharaux, Pierre-Louis, additional

Published
2011
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9. Malignant Germ Cell–Like Tumors, Expressing Ki-1 Antigen (CD30), Are Revealed during in VivoDifferentiation of Partially Reprogrammed Human-Induced Pluripotent Stem Cells

Author

Griscelli, Frank, Féraud, Olivier, Oudrhiri, Noufissa, Gobbo, Emilie, Casal, Ibrahim, Chomel, Jean-Claude, Biéche, Ivan, Duvillard, Pierre, Opolon, Paule, Turhan, Ali G., and Bennaceur-Griscelli, Annelise

Abstract

Because many of the genes used to produce induced pluripotent stem cells (iPSCs) from somatic cells are either outright established oncogenes, such as c-mycand Klf4, or potentially related to tumorigenesis in various cancers, both the safety and the risks of tumorigenesis linked to iPSC generation require evaluation. In this work, we generated, by lentivirus-mediated gene transfer of Oct4, Sox2, Nanog, and Lin28, two types of iPSCs from human mesenchymal stem cells and human amniotic fluid–derived cells: fully reprogrammed iPSCs with silencing of the four transgenes and partially reprogrammed iPSCs that still express one or several transgenes. We assessed the behavior of these cells during both their differentiation and proliferation using in vivoteratoma assays in nonobese diabetic mice with severe combined immunodeficiency. In contrast to fully reprogrammed iPSCs, 43% of partially reprogrammed iPSC cases (6 of 14 teratomas) generated major dysplasia and malignant tumors, with yolk sac tumors and embryonal carcinomas positive for α-fetoprotein, cytokeratin AE1/AE3, and CD30. This correlated with the expression of one or several transgenes used for the reprogramming, down-regulation of CDK 1A mRNA (p21/CDKN1A), and up-regulation of antiapoptotic Bcl-2 mRNA. Therefore, the oncogenicity of therapeutically valuable patient-specific iPSC-derived cells should be scrupulously evaluated before they are used for any clinical applications.

Published
2012
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