Team members

SCHANSTRA
Joost-Peter
(DR1)

SCHANSTRA Joost-Peter (DR1)

joost-peter.schanstra@inserm.fr

+ 33531224078

PhD, Director of research, Group leader





Road walked on:


Joost Schanstra received his PhD in Biochemistry from the University of Groningen, Groningen, The Netherlands, in 1996. From 1996 to 1999 he worked as a post-doctoral fellow in the field of Nephrology and was recruited as a Principal investigator at INSERM, Toulouse, in 1999. Since 2008, Joost Schanstra is a Director of research at the Renal Fibrosis Lab, INSERM U1048.





Main domains of expertise:


Clinical proteomics, Chronic kidney disease, Systems biology, Urinary biomarkers





Selected Publications:


Diagnosis and Prediction of CKD Progression by Assessment of Urinary Peptides. Schanstra JP, Zürbig P, Alkhalaf A, Argiles A, Bakker SJ, Beige J, Bilo HJ,Chatzikyrkou C, Dakna M, Dawson J, Delles C, Haller H, Haubitz M, Husi H,Jankowski J, Jerums G, Kleefstra N, Kuznetsova T, Maahs DM, Menne J, Mullen W,Ortiz A, Persson F, Rossing P, Ruggenenti P, Rychlik I, Serra AL, Siwy J,Snell-Bergeon J, Spasovski G, Staessen JA, Vlahou A, Mischak H, Vanholder R. J Am Soc Nephrol. 2015. [Read]





Fetal urinary peptides to predict postnatal outcome of renal disease in fetuses with posterior urethral valves (PUV). Klein J, Lacroix C, Caubet C, Siwy J, Zürbig P, Dakna M, Muller F, Breuil B, Stalmach A, Mullen W, Mischak H, Bandin F, Monsarrat B, Bascands JL, Decramer S, Schanstra JP. Sci Transl Med. 2013 Aug 14;5(198):198ra106. [Read]





Predicting the clinical outcome of congenital unilateral ureteropelvic junction obstruction in newborn by urinary proteome analysis. Decramer S, Wittke S, Mischak H, Zürbig P, Walden M, Bouissou F, Bascands JL, Schanstra JP. Nat Med. 2006 Apr;12(4):398-400. [Read]





In vivo bradykinin B2 receptor activation reduces renal fibrosis. Schanstra JP, Neau E, Drogoz P, Arevalo Gomez MA, Lopez Novoa JM, Calise D, Pecher C, Bader M, Girolami JP, Bascands JL. J Clin Invest. 2002 Aug;110(3):371-9. [Read]





Kinetics of halide release of haloalkane dehalogenase: evidence for a slow conformational change. Schanstra JP, Janssen DB. Biochemistry. 1996 May 7;35(18):5624-32. [Read]
AMAYA-GARRIDO
Ana
(Doc)

AMAYA-GARRIDO Ana (Doc)

ana.amaya-garrido@inserm.fr

+33531224084

ALVES
Melinda
(IE)

ALVES Melinda (IE)

melinda.alves@inserm.fr

+33531224077

BREUIL
Benjamin
(AI)

BREUIL Benjamin (AI)

breuil.benjamin@inserm.fr

+33 531224077

Road walked on:

Benjamin Breuil received his technical degree in France, in 1998. From 1999 to 2008 he worked as an assistant engineer in food security and pharmaceutical companies and acquired differents skills in analytical chemistry, robotic and transcriptomics. Recruited permanently at INSERM in 2014, Benjamin Breuil is an assistant engineer at the Renal Fibrosis Lab, INSERM U1048 since 2008.



Main domains of expertise:

Urinary biomarker, Clinical proteomics, Metabolomics, Mass spectrometry, Capillary electrophoresis



Selected Publications:

Label-free quantitative urinary proteomics identifies the arginase pathway as a new player in congenital obstructive nephropathy. Lacroix C, Caubet C, Gonzalez-de-Peredo A, Breuil B, Bouyssié D, Stella A, Garrigues L, Le Gall C, Raevel A, Massoubre A, Klein J, Decramer S, Sabourdy F, Bandin F, Burlet-Schiltz O, Monsarrat B, Schanstra JP, Bascands JL. Mol Cell Proteomics. 2014. [Read]



Fetal urinary peptides to predict postnatal outcome of renal disease in fetuses with posterior urethral valves (PUV). Klein J, Lacroix C, Caubet C, Siwy J, Zürbig P, Dakna M, Muller F, Breuil B, Stalmach A, Mullen W, Mischak H, Bandin F, Monsarrat B, Bascands JL, Decramer S, Schanstra JP. Sci Transl Med. 2013. [Read]



Long term metabolic syndrome induced by a high fat high fructose diet leads to minimal renal injury in C57BL/6 mice. Dissard R, Klein J, Caubet C, Breuil B, Siwy J, Hoffman J, Sicard L, Ducassé L, Rascalou S, Payre B, Buléon M, Mullen W, Mischak H, Tack I, Bascands JL, Buffin-Meyer B, Schanstra JP. PLoS One. 2013. [Read]
BUFFIN-MEYER
Bénédicte
(MCU)

BUFFIN-MEYER Bénédicte (MCU)

benedicte.buffin-meyer@inserm.fr

+33 531224076

PhD, Associate professor, Principal investigator

Road walked on:
Bénédicte Buffin-Meyer received her PhD from the University of Paris-Sud/Orsay, Paris, France, in 1996 in the field of Nephrology. From 1997 to 1999 she worked as a post-doctoral researcher and was recruited as Associate Professor in Physiology at University Paul Sabatier, Toulouse, in 1999. Since 2007, Bénédicte Buffin-Meyer is a principal investigator at the Renal Fibrosis Lab, INSERM U1048.

Main domains of expertise:
Renal cellular biology, Kidney disease, Metabolomics, Urinary shear stress

Selected Publications:
Shear stress-induced alteration of epithelial organization in human renal tubular cells. D Maggiorani, R Dissard, M Belloy, JS Saulnier-Blache, A Casemayou, L Ducasse, S Grès, J Bellière, C Caubet, JL Bascands, JP Schanstra, B Buffin-Meyer. PLoS One. 2015 Jul 6;10(7):e0131416, 2015.

Renal tubular fluid shear stress facilitates monocyte activation towards inflammatory macrophages. M Miravète, R Dissard, J Klein, J Gonzalez, C Caubet, C Pecher, B Pipy, JL Bascands, M Mercier-Bonin, JP Schanstra, B Buffin-Meyer. Am J Physiol Renal Physiol. 2012 Jun 1;302(11):F1409-17.

Renal tubular fluid shear stress promotes endothelial cell activation. M Miravète, J Klein, A Besse-Patin, J Gonzalez, C Pecher, JL Bascands, M Mercier-Bonin, JP Schanstra, B Buffin-Meyer. Biochem Biophys Res Commun. 2011 Apr 22;407(4):813-7.

Differential regulation of collecting duct Na+, K+-ATPase and K+ excretion by furosemide and piretanide: role of bradykinin. B Buffin-Meyer, M Younes-Ibrahim, G El Mernissi, L Cheval, S Marsy, M Grima, JP Girolami, A Doucet. J Am Soc Nephrol. 2004 15, 876-884.

Regulation of Na+, K(+)-ATPase in the rat outer medullary collecting duct during potassium depletion. B Buffin-Meyer, JM Verbavatz, L Cheval, S Marsy, M Younes-Ibrahim, C Le Moal, A Doucet. J Am Soc Nephrol. 1998 9: 538-550.
BULÉON
Marie
(IE)

BULÉON Marie (IE)

marie.buleon@inserm.fr

+33531224077

CADOUOT
Mégane
(Stagiaire)

CADOUOT Mégane (Stagiaire)

megane.cadouot@inserm.fr

+33531224077

CASEMAYOU
Audrey
(IE)

CASEMAYOU Audrey (IE)

audrey.casemayou@inserm.fr

+33 531224080

Road walked on:
Audrey Casemayou received her PhD from the University Paul Sabatier,Toulouse, France, in 2010. From 2006 to 2010 she worked as a PhD student in the field of regulatory T cells and experimental autoimmune encephalomyelitis. Since 2011 she worked as a post-doctoral researcher in the field of HNF1B and acute renal diseases at the Renal Fibrosis Lab, INSERM U1048.

Main domains of expertise:
Acute kidney disease, Cellular biology, HNF1beta, Molecular biology, Renal fibrosis mechanisms

Selected Publications:
Specific macrophage subtypes influence the progression of rhabdomyolysis-induced kidney injury. Belliere J, Casemayou A, Ducasse L, Zakaroff-Girard A, Martins F, Iacovoni JS, Guilbeau-Frugier C, Buffin-Meyer B, Pipy B, Chauveau D, Schanstra JP, Bascands JL. J Am Soc Nephrol. 2015. [Read]

Tocilizumab added to conventional therapy reverses both the cytokine profile and CD8+Granzyme+ T-cells/NK cells expansion in refractory hemophagocytic lymphohistiocytosis. Faguer S, Vergez F, Peres M, Ferrandiz I, Casemayou A, Belliere J, Cointault O, Lavayssiere L, Nogier MB, Prevot G, Huart A, Recher C, Rostaing L. Hematol Oncol. 2014. [Read]

The HNF1B score is a simple tool to select patients for HNF1B gene analysis. Faguer S, Chassaing N, Bandin F, Prouheze C, Garnier A, Casemayou A, Huart A, Schanstra JP, Calvas P, Decramer S, Chauveau D. Kidney Int. 2014. [Read]

Hnf-1β transcription factor is an early hif-1α-independent marker of epithelial hypoxia and controls renal repair. Faguer S, Mayeur N, Casemayou A, Pageaud AL, Courtellemont C, Cartery C, Fournie GJ, Schanstra JP, Tack I, Bascands JL, Chauveau D. PLoS One. 2013. [Read]

The p.Arg63Trp polymorphism controls Vav1 functions and Foxp3 regulatory T cell development. Colacios C, Casemayou A, Dejean AS, Gaits-Iacovoni F, Pedros C, Bernard I, Lagrange D, Deckert M, Lamouroux L, Jagodic M, Olsson T, Liblau RS, Fournié GJ, Saoudi A. J Exp Med. 2011. [Read]
CHAUBET
Adeline
(AI)

CHAUBET Adeline (AI)

adeline.chaubet@inserm.fr

+33531224077

CHAUVEAU
Dominique
(PU-PH)

CHAUVEAU Dominique (PU-PH)

chauveau.d@chu-toulouse.fr

DENIS
Colette
(MCU)

DENIS Colette (MCU)

colette.denis@inserm.fr

+33 531224076

PhD, Associate professor, Principal investigator

Road walked on:
Colette Denis received her PhD from the University Paul Sabatier, Toulouse, France, in 1985 and was recruited as an Associate Professor at University Paul Sabatier in 1988. From 1983 to 1990 she worked on the regulation of glycolysis in intestinal adenocarcinoma cells, and from 1990 to 2004 she specialized in molecular pharmacology. Since 2015, Colette Denis is a principal investigator at the Renal Fibrosis Lab, INSERM U1048.

Main domains of expertise:
Pharmacology, Efficacy of biased ligands, Cellular biology, Plasma /urine biochemistry

Selected Publications:
Dual agonist occupancy of AT1-R-α2C-AR heterodimers results in atypical Gs-PKA signaling. Bellot M, Galandrin S, Boularan C, Matthies HJ, Despas F, Denis C, Javitch J, Mazères S, Sanni SJ, Pons V, Seguelas MH, Hansen JL, Pathak A, Galli A, Sénard JM, Galés C. Nat Chem Biol. 2015, 11, 271-281.

Delineating the complexity of biased and full agonism reveals the existence of a new distinct active AT1 receptor entity. A. Saulière, M. Bellot, H. Paris, C. Denis, F. Finana, J. T. Hansen, M.F. Altié, M.H. Seguelas, J.L. Hansen, J.M. Sénard & C. Galés. Nat. Chem. Biol. 2012, 8, 622-30.

Probing heterotrimeric G protein activation: applications to biased ligands. C. Denis, A. Saulière, S. Galandrin, JM Senard & C. Galés. Curr. Pharm. Des. 2012, 18, 128-44.

Interest of alpha2-adrenergic agonists and antagonists in clinical practice: background, facts and perspectives. P.A. Crassous, C. Denis, H. Paris & J.M. Senard. Curr. Top. Med. Chem. 2007, 7, 187-94.

Alpha2-adrenoceptors regulate proliferation of human intestinal epithelial cells. S. Schaak, D. Cussac, C. Cayla, J.C. Ddevedjian, R. Guyot, H. Paris & C. Denis. Gut, 2000, 47, 242-250.
FEDOU
Camille
(Doc)

FEDOU Camille (Doc)

camille.fedou@inserm.fr

+33531224084

FAGUER
Stanislas
(PU-PH)

FAGUER Stanislas (PU-PH)

stanislas.faguer@inserm.fr

+33531224080

FEUILLET
Guylène
(IE)

FEUILLET Guylène (IE)

guylene.feuillet@inserm.fr

DECRAMER
Stéphane
(PU-PH)

DECRAMER Stéphane (PU-PH)

decramer.s@chu-toulouse.fr

Medical Doctor



Stéphane’s professional interest:



Stéphane Decramer (MD) is working both as a clinician (paediatric nephrologist) in the children’s hospital of Toulouse and as a scientist at the French institute of health and medical research (INSERM). He has extensive experience in the field of developmental nephropathies, identification of gene-anomalies, and clinical proteomics.



KLEIN
Julie
(CR-CN)

KLEIN Julie (CR-CN)

julie.klein@inserm.fr

+33 531224076

PhD, Researcher, Principal investigator

http://cvscience.aviesan.fr/cv/1705/julie-klein

Road walked on:
Julie Klein received her PhD from the University Paul Sabatier, Toulouse, France, in 2009. From 2009 to 2014 she worked as a post-doctoral fellow in the field of proteomics and bioinformatics in chronic kidney disease and was recruited as a researcher at the Renal Fibrosis Lab, INSERM U1048, Toulouse in 2014.

Main domains of expertise:
Bioinformatics tools and databases (KUPKB, Proteasix), Clinical proteomics, Cardiovascular complications of chronic kidney disease, Mechanisms of chronic kidney disease, Urinary biomarkers

Selected Publications:
New insights in molecular mechanisms involved in chronic kidney disease using high-resolution plasma proteome analysis. Glorieux G, Mullen W, Duranton F, Filip S, Gayrard N, Husi H, Schepers E, Neirynck N, Schanstra JP, Jankowski J, Mischak H, Argilés A, Vanholder R, Vlahou A, Klein J. Nephrol Dial Tranplant. 2015.

Urinary proteomics and molecular determinants of chronic kidney disease: possible link to proteases. Filip S, Pontillo C, Peter Schanstra J, Vlahou A, Mischak H, Klein J. Expert Rev Proteomics. 2014 Oct;11(5):535-48. doi: 10.1586/14789450.2014.926224. Epub 2014 Jun 24.

Fetal urinary peptides to predict postnatal outcome of renal disease in fetuses with posterior urethral valves (PUV). Klein J, Lacroix C, Caubet C, Siwy J, Zürbig P, Dakna M, Muller F, Breuil B, Stalmach A, Mullen W, Mischak H, Bandin F, Monsarrat B, Bascands JL, Decramer S, Schanstra JP. Sci Transl Med. 2013 Aug 14;5(198):198ra106. doi: 10.1126/scitranslmed.3005807.

Proteasix: a tool for automated and large-scale prediction of proteases involved in naturally-occurring peptide generation. Klein J, Eales J, Zurbig P, Vlahou T, Mischak H, Stevens R. Proteomics, 2013 Apr;13(7):1077-82. doi: 10.1002/pmic.201200493. Epub 2013 Feb 26.

The KUPKB: a novel Web application to access multiomics data on kidney disease. Klein J, Jupp S, Moulos P, Fernandez M, Buffin-Meyer B, Casemayou A, Chaaya R, Charonis A, Bascands JL, Stevens R, Schanstra JP. FASEB J. 2012 May;26(5):2145-53. doi: 10.1096/fj.11-194381. Epub 2012 Feb 17.
LESCAT
Ophélie
(IE)

LESCAT Ophélie (IE)

NEAU
Eric
(IE)

NEAU Eric (IE)

eric.neau@inserm.fr

+33531224077

Road walked on:
Eric Neau received his master degree in cellular biology, option genetics from the University Pierre and Marie Curie, Paris, France, in 1988. From 1991 to 1999 he worked as an assistant engineer in the field of gene expression IGFBP1 (insulin-like growth factor binding protein 1) in liver and was recruited as an assistant engineer at INSERM, Toulouse, in 1999. Since 2008, Eric Neau is a research engineer at the Renal Fibrosis Lab, INSERM U1048.

Main domains of expertise:
Molecular biology, Quantitative PCR, miRNA

Selected Publications:
miRNAs in urine: a mirror image of kidney disease? Papadopoulos T, Belliere J, Bascands JL, Neau E, Klein J, Schanstra JP. Expert Rev Mol Diagn. 2015 Mar;15(3):361-74. [Read]

Blockade of the kinin B1 receptor ameloriates glomerulonephritis. Klein J, Gonzalez J, Decramer S, Bandin F, Neau E, Salant DJ, Heeringa P, Pesquero JB, Schanstra JP, Bascands JL. J Am Soc Nephrol. 2010 Jul;21(7):1157-64. [Read]

Gene expression profiling in the remnant kidney model of wild type and kinin B1 and B2 receptor knockout mice. JP Schanstra, M Bachvarova, E Neau, JL Bascands, D Bachvarov. Kidney Int. 2007, Aug 72(4):442-54. [Read]

In Vivo bradykinin B2 receptor activation reduces renal fibosis. Schanstra JP, Neau E, Drogoz P, Arevalo Gomez MA, Lopez Novoa JM, Calise D, Pecher C, Bader M, Girolami JP, Bascands JL. J Clin Invest. 2002, Aug ; 110(3) : 371-9. [Read]

The glucocorticoid response element II is functionally homologous in rat and human insulin-like growth factor-binding protein-1 promoters. Schweizer-Groyer G, Jibard N, Neau E, Fortin D, Cadepond F, Baulieu EE, Groyer A. J Biol Chem. 1999, April 23, 274, 17: 11679-88. [Read]
PIEDRAFITA
Alexis
(Doc)

PIEDRAFITA Alexis (Doc)

Alexis.piedrafita@inserm.fr

SAULNIER-BLACHE
JS
(DR2)

SAULNIER-BLACHE JS (DR2)

jean-sebastien.saulnier-blache@inserm.fr

+33531224076

PhD, Director of research, Principal investigator







Road walked on:



Jean Sébastien Saulnier-Blache received his PhD from the University Paul Sabatier, Toulouse, France, in 1990. He was recruited at INSERM as a researcher in 1992 and promoted as director of research in 2005. From 1992 to 1994 he worked in the field of molecular biology at the University of South Carolina, Charleston, SC, USA. From 1994 to 2014 he worked in the field of Obesity and Diabetes at INSERM Toulouse. Since 2014, Jean Sébastien Saulnier-Blache is a principal investigator at the Renal Fibrosis Lab, INSERM U1048.







Main domains of expertise:



Cellular biology, Clinical lipidomics, Diabetic nephropathy, Lysophosphatidic acid, Renal fibrosis mechanisms







Selected Publications:



Pro-fibrotic activity of lysophosphatidic acid in adipose tissue: in vivo and in vitro evidence. Rancoule C, Viaud M, Gres S, Viguerie N, Decaunes P, Bouloumié A, Langin D, Bascands JL, Valet P, Saulnier-Blache JS. Biochim Biophys Acta. 2014 Jan;1841(1):88-96.







Lysophosphatidic acid impairs glucose homeostasis and inhibits insulin secretion in high-fat diet obese mice. Rancoule C, Attané C, Grès S, Fournel A, Dusaulcy R, Bertrand C, Vinel C, Tréguer K, Prentki M, Valet P, Saulnier-Blache JS. Diabetologia. 2013 Jun;56(6):1394-402.







Adipose-specific disruption of autotaxin enhances nutritional fattening and reduces plasma lysophosphatidic acid. Dusaulcy R, Rancoule C, Grès S, Wanecq E, Colom A, Guigné C, van Meeteren LA, Moolenaar WH, Valet P, Saulnier-Blache JS. J Lipid Res. 2011 Jun;52(6):1247-55.







LPA1 receptor activation promotes renal interstitial fibrosis. Pradère JP, Klein J, Grès S, Guigné C, Neau E, Valet P, Calise D, Chun J, Bascands JL, Saulnier-Blache JS, Schanstra JP. J Am Soc Nephrol. 2007 Dec;18(12):3110-8.







Potential involvement of adipocyte insulin resistance in obesity-associated up-regulation of adipocyte lysophospholipase D/autotaxin expression. Boucher J, Quilliot D, Pradères JP, Simon MF, Grès S, Guigné C, Prévot D, Ferry G, Boutin JA, Carpéné C, Valet P, Saulnier-Blache JS. Diabetologia. 2005 Mar;48(3):569-77.
TACK
Yvan
(PU-PH)

TACK Yvan (PU-PH)

tack.i@chu-toulouse.fr

In 2017, on a world scale the total number of individuals with chronic kidney disease (CKD), acute kidney injury (AKI), and those on renal replacement therapy (RRT) exceeded 850 million, a truly concerning figure that is twice the estimated number of people with diabetes worldwide and >20 times higher than the number of individuals affected by AIDS/HIV worldwide (Jager KJ, Kidney Int. 2019). We aim to contribute to reduce the burden of kidney disease by focusing on the following topics.

1) Early and non-invasive detection of CKD. Late stage CKD is very difficult to treat and the "Holy Grail" remains early disease detection since standard of care medication, such as inhibitors of the renin angiotensin system, are generally quite effective in delaying the progression of the disease. In children, CKD is frequently related to abnormal kidney development, while in adults this essentially results from diabetes and aging. We focus on early disease detection using “omics” approaches to identify biomarkers in body fluids such as urine, blood and amniotic fluid. In addition to their contribution to early detection of CKD, these omics-related markers are also analyzed for the potential involvement in the pathophysiology of the disease using models systems. Our ultimate goal is to provide early CKD detection tests for the clinic, provide innovative therapeutic strategies and improve its management. To achieve these goals, we have access to several thousand samples and follow-up data of adult and pediatric patients and a wide panel of model systems.

2) Early detection of AKI and improvement of treatment. AKI is a common complication in hospitalized patients. It is associated with an increased risk of early and late mortality, as well as the development of CKD among survivors. The absence of AKI predictors (before renal aggression) and of early and robust AKI biomarkers (4 to 6 hours after aggression) do not allow to stratify the patients upstream or immediately after renal aggression and according to the risk of AKI. It is therefore essential to improve this stratification (in particular pre-aggression) in order to personalize the management and to offer a specific treatment only to patients at risk of or developing AKI. Such optimized stratification should also facilitate the identification of new treatments and reduce the number of patients to include in interventional clinical studies. It will finally identify a panel of biomarkers that can be used in humans or animals to promote the transferability of a molecule from animals to humans.

3) Reduce cardiovascular complications. CKD is associated with a very high risk of cardiovascular mortality (CV). However, the mechanisms of the cardiovascular complications of CKD are atypical and therefore still poorly understood. In particular, atheroma plaques in CKD patients are defined by the aberrant development of compromised blood vessels and micro-calcifications. In addition, cardiovascular lesions appear in a silent manner and are generally detected only at an advanced stage, at the time of the occurrence of a CV event. It is therefore essential to better understand the pathophysiology of CV complications, but also to identify at an early stage CKD patients at risk for CV complications in order to improve their management and to individualize their medical follow-up. This research is expected to improve the quality of life of many patients with CKD, allowing older people who are severely affected by this disease to age better.

Focus on omics. Much of our research is based on data obtained by omic approaches because it has been shown that complex pathologies, such as nephropathies, cannot be described by one or two markers only. We are therefore working towards the detection of molecular signatures of kidney disease that may be mono-omic (Decramer et al., Nat Med 2006, Klein et al., Sci Transl Med 2013) or multi-omic to further improve the description of this complex pathology. These omics approaches are also useful for: i) discovering new drugs through drug repositioning as we have recently shown (Schanstra et al., JCI-Insight 2019); ii) improve the translatability of preclinical observations by the generation of humanized non-invasive signatures in animals (Klein et al., Kidney Int 2016); iii) identify new targets both in the area of ​​cardiovascular complications and of renal development.

Humanization

Expected benefits
- Non-invasive diagnostic tests for early detection of kidney disease, progression and complications.
- Specific targets (drugs) and appropriate management to prevent the development and complications of kidney disease.