Dr. Pierre-Louis Tharaux

CV

Current position

Inserm Research Professor and Team leader, Paris Cardiovascular Research Centre - PARCC, 56 rue Leblanc, 75015 Paris and lecturer (AP-HP-Inserm) at the Nephrology Dpt, Hôpital Européen Georges Pompidou (HEGP), Paris.

Education and Training

• Medical studies at Faculté Necker-Enfants Malades- Université Paris Descartes (1983-1990).
• Interne des Hôpitaux de Paris (1991)
• Fellowship in Nephrology (1991-1998). Nephrology: Board Certified (1998).
• Medical Doctorate from University Paris Descartes (1998). Suma cum laude
• PhD. in Physiology & Pathophysiology from University Pierre & Marie Curie (2000), Paris. Suma cum laude.

Professional Experiences

• 1990-1996 : “Internat de Médecine” (Residency and Fellowship equivalent) in Paris : (ICU, nephrology, hepatology, endocrinology, physiology).
• 1997-2000 : Research: Internat of Paris Fellowship, Silver medal award of Assistance Publique-Hôpitaux de Paris, INSERM fellowship for biomedical research.
• 2000-2002 : Research Associate, Duke University Medical Center, Durham, NC,  Dr Thomas M Coffman laboratory and University of North Carolina, Dr Beverly Koller lab. Fellow of the Simone and Cino del Duca Fundation and Elli-Lilly International fellow.
• 2002- present: INSERM Investigator.
• 2009- present: Inserm Research Director (Research Professor) and team leader, Paris Cardiovascular Research Center @ HEGP, Inserm.

Honors-Awards

• Clinical research fellowship for excellence in Medicine – 1995
• Silver medal for Interns in Paris Public teaching hospitals, AP-HP, 1997
• INSERM fellowship for biomedical research – 1998
• Louis Auquier / AP-HP award for Academic Achievement in Medicine - 1999
• European Research Council Starting Grant award 2012
• Eloi Collery Prize of the French National Academy of Medicine – 2013

Selected Publications

• Nrf2 drives podocyte-specific PPARg expression that is essential to promote resistance to crescentic glomerulonephritis Henique C*, Bollee G*, Lenoir O, Dhaun N, Camus M, Chipont A, Flosseau K, Mandet C, Yamamoto M, Karras A, Thervet E, Bruneval P, Nochy D, Mesnard L, Tharaux P-L. J Am Soc Nephrol. 2015, in press
• Endothelial cell- and podocyte autophagy synergistically protect from diabetes-induced glomerulosclerosis Lenoir O , Jasiek M, Hénique C, Guyonnet L, Hartleben B, Bork T, Chipont A,  Flosseau K, Bensaada I, Schmitt A, Massé JM,  Souyri  M, Huber TB, Tharaux PL. Autophagy. 2015 ;11(7):1130-45. doi: 10.1080/15548627.2015.1049799.

• Direct action of endothelin-1 on podocytes promotes diabetic glomerulosclerosis. Lenoir O, Milon M, Virsolvy A, Hénique C, Schmitt A, Massé JM, Kotelevtsev Y, Yanagisawa M, Webb DJ, Richard S, Tharaux PL. J Am Soc Nephrol. 2014;25(5):1050-62.
• The Epidermal Growth Factor Receptor Promotes Glomerular Injury and Renal Failure in Rapidly Progressive Crescentic Glomerulonephritis. Bollée G and Flamant M, Schordan S, Fligny C, Rumpel E, Milon M, Schordan E, Sabaa N, Vandermeersch S, Galaup A, Rodenas A, Casal I, Sunnarborg Susan W, Salant DJ, Kopp JB, Threadgill DW, Quaggin SE, Dussaule JC, Germain S, Mesnard L, Endlich K, Boucheix C, Belenfant X, Callard P, Endlich N, Tharaux PL. Nat Med. 2011;17(10):1242-50. doi: 10.1038/nm.2491

• Single europium-doped nanoparticles measure temporal pattern of reactive oxygen species production inside cells. Casanova D, Bouzigues C, Nguyên TL, Ramodiharilafy RO, Bouzhir-Sima L, Gacoin T, Boilot JP, Tharaux PL, Alexandrou A. Nat Nanotechnol. 2009; 4(9):581-5.

FRIAS Research Project

Determinants of metabolic switches and cell death of glomerular cells in Focal Segmental Glomerulosclerosis and Ageing

Glomerular diseases (GD) encompass a broad array of clinicopathologically defined syndromes which together account for 90% of end-stage kidney disease costing € 16 billion per annum to treat in the EU alone. Recent insights have defined the central role of the podocyte as both the regulator of glomerular development as well as the determinant of progression to glomerulosclerosis and renal failure. We are numbering the GPCRs in normal and diseased podocytes and established that EGFR is transactivated by Gq-coupled GPCRs in these cells. We shall determine whether behavior of these cells is influenced by activation of the identified receptors in vitro. In GD, podocytes may undergo detachment, apoptosis, proliferation or migration. Using podocytes from glomerular explants, we will address the effects of GPCR agonists on in vitro models of each of these changes.

We will study the extracellular stimuli that elicit pathological changes in autophagosome Golgi/ER crosstalk in podocytes. This research axis synergize with research performed by Dr. Jörn Dengjel.

We will investigate mechanisms promoting podocyte aging and death. Autophagy is blocked in an age dependent manner by unknown mechanisms. Our data suggest that some GPCRs contribute to this phenomenon. Interaction with cellular respiration is suggested by our preliminary findings. This will be optimally studied with Pr. Tobias Huber Lab.

At last, we will study genomic and miRNA signature of podocytes from young and ageing mice with common co-morbid conditions such as hypertension and diabetes.