Gerard Friedlander MD, PhD. Professor of Physiology
Course and current status
Name : Gérard FRIEDLANDER, M.D., Ph.D.
Date and place of birth: June 18, 1952, Paris, France
Professional Address Inserm U845 Research Center “Growth and Signaling”
Faculté de Médecine Paris Descartes, site Necker
156, rue de Vaugirard, 75730 Paris Cedex 15, France
Tel. +33 1 40 61 53 10 ; Fax +33 1 43 06 04 43 gerard.friedlander@inserm.fr
Present position
Hospital functions
Head, Department of Physiology & Radio-isotopes - Hôpital Européen Georges-Pompidou,
20, rue Leblanc - 75015 Paris - Tel. 01 56 09 39 69 gerard.friedlander@egp.aphp.fr
Research functions
Director, Research Center “Growth and Signaling” Inserm U845 & Dept. of Physiology, Paris Descartes University
Teaching activities
Professor of Physiology; Paris Descartes Medical School
Postgraduate training
1969 - 1975 M.D. Faculté Saint-Antoine, Pierre et Marie Curie University Paris, France
1980 - 1984 Ph.D. (Physiology) - Denis Diderot (Paris 7) University, Paris, France
Professional Experience and Positions held
1977 - 1981 Resident physician, Paris
1982 - 1989 Assistant Professor of Physiology, Director: Pr Claude Amiel,
Bichat Hospital, Paris
1989 - 2004 Professor of Physiology, Dept of Physiology and Bichat hospital, Paris 7 University
1995 - 2005 Director of research unit Inserm 426
Awards and Honors
2002 Eloi Collery Award of the National Academy of Medicine
2001 Chevalier dans l'ordre de la Légion d'Honneur
Scientific societies
National Academy of Medicine
French Speaking Society of Nephrology
French Society of Physiology
European Society of Nephrology
American Society of Nephrology
International Society of Nephrology
European Dialysis and Transplant Association – European Renal Association
Academia Europaea
American Society of Bone and Mineral Research
Editorship and editorial boards
2007 - Member of the Editorial Board, Kidney International
2002 - 2006 Editor in chief, Medecine-Sciences
2000 - Associate Editor, Nephrology, Dialysis, Transplantation
Boards and Committees
International Committees
1993 - 1997 Councillor, European Society for Clinical Investigation
1996 - 1999 Councillor, European Kidney Research Forum
2003 - 2007 Councillor, European Kidney Research Association
French Committees
1994 - 1997 Chairman, Pedagogic Council, Xavier-Bichat Faculty
1999 - 2002 Councillor, Scientific Committee,
Fondation pour la Recherche Médicale (Medical Research Foundation)
1999 - 2002 Chairman, INSERM Committee n°7
(Nephrology, Gastroenterology, Dermatology)
2002 - 2004 Member, Administrative council, University Paris7
2005 - 2007 Member, Administrative council, Paris Descartes University
2008 - Member, Scientific council, Paris Descartes University
2008 - Vice-Dean, Paris Descartes School of Medicine
Main publications (limited to 10)
Prié D, Friedlander G. Genetic disorders of renal phosphate transport. N Engl J Med, 2010, 362, 2399-409
Karim Z, Gérard B, Bakouh N, Alili R, Leroy C, Beck L, Silve C, Planelles G, Urena-Torres P, Grandchamp B, Friedlander G, Prié D. Human NHERF1 mutations and renal parathyroid hormone responsiveness. New Engl J Med, 2008, 359, 1128-35.
Lautrette A, Li S, Alili R, Sunnarborg SW, Burtin M, Lee DC, Friedlander G, Terzi F Angiotensin II and EGF receptor cross-talk in chronic kidney diseases: a novel therapeutic approach. Nat Med 2005, 11, 867-74.
Pillebout E, Weitzman JB, Burtin M, Martino C, Federici P, Yaniv M, Friedlander G, Terzi F. JunD protects against chronic kidney disease by regulating paracrine mitogens. J Clin Invest. 2003, 112, 843-852.
Prie D, Huart V, Bakouh N, Planelles G, Dellis O, Gerard B, Hulin P, Benque-Blanchet F, Silve C, Grandchamp B, Friedlander G. Nephrolithiasis and osteoporosis associated with hypophosphatemia caused by mutations in the type 2a sodium-phosphate cotransporter. N Engl J Med, 2002, 347, 983-991
Terzi F, Burtin M, Hekmati M, Federici P, Grimber G, Briand P, Friedlander G. Targeted expression of a dominant-negative EGF-R in the kidney reduces tubulo-interstitial lesions after renal injury. J Clin Invest, 2000, 106, 225-234
Essig M, Nguyen G, Prié D, Escoubet B, Sraer JD, Friedlander G. 3-Hydroxy-3-Methylglutaryl Coenzyme A reductase inhibitors increase fibrinolytic activity in rat aortic endothelial cells. Circ Res, 1998, 83, 683-690
Terzi F, Henrion D, Colucci-Guyon E, Federici P, Babinet C, Levy BI, Briand P, Friedlander G. Reduction of renal mass is lethal in mice lacking vimentin. Role of endothelin-nitric oxide imbalance. J Clin Invest, 1997, 100, 1520-1528.
Fernandes I, Hampson G, Cahours X, Morin P, Coureau C, Couette S, Prié D, Biber J, Murer H, Friedlander G, Silve C. Abnormal sulfate metabolism in vitamin D-deficient rats. J Clin Invest, 1997, 100, 2196-2203.
Friedlander G, Couette S, Coureau C, Amiel C. Mechanisms whereby extracellular adenosine 3',5'-monophosphate inhibits phosphate transport in cultured opossum kidney cells and in rat kidney. Physiological implication. J Clin Invest, 1992, 90, 848-858.
Scientific summary
Phosphate (Pi) homeostasis has a central place in metabolism, cellular proliferation, development, and bone mineralization. Pi homeostasis relies on a coordinate function of membrane transporters (ubiquitous PiT, epithelial NPT), of intracellular regulatory proteins and of endocrine and paracrine modulators.
Our purpose is to study Pi homeostasis at the level of the cell and of the whole organism, both in normal and pathological situations.
Cellular Pi homeostasis
Cellular and molecular Pi physiology
. We propose (a) to investigate the specificity of PiT1 and PiT2 expression in response to transcription factors and growth factors through promoter studies; (b) to get insights into the mechanisms underlying the role of PiT1 in cell proliferation and modulation of the cell cycle; (c) to evaluate the role of PiT1 and PiT2 as Pi sensors.
Consequences of PiT1 invalidation.
We shall evaluate, in vivo, the phenotypic consequences of PiT knockout (allelic series obtained by homologous recombination) or conditional invalidation (cre-lox) in the mouse: (a) during development, focusing on bone, liver and kidney; (b) in pathological situations (renal acute and chronic injury, liver regeneration and hepatocarcinoma.
Phosphate homeostasis at the organism level
This clinical research aims to : (a) dissect at the molecular level renal Pi leaks which lead to renal stones and bone loss: identification and characterization (heterologous expression) of mutations affecting renal transporters NPT2a, NPT2c, and regulatory proteins NHERF1 and NHERF2; (b) look for structure/secretion abnormalities of phosphaturic peptides such as FGF23; evaluate the implication of klotho, a recently identified gene involved in cardiovascular aging, in end stage renal failure-associated hyperphosphatemia and in vitamin D metabolism.
This project, which combines experimental and clinical research, takes place in the context of the renewal of the “Growth and Signaling” Inserm Research Center U845 on the Necker campus. It involves 1 full-time scientist (CR1), 4 hospital/university investigators, 3 engineers and technicians, 2 post-docs and 3 PhD students.
