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Article ; Online: Neuropilin-1 regulates renin synthesis in juxtaglomerular cells.

Shen, Yunzhu / Lotenberg, Kenza / Zaworski, Jeremy / Broeker, Katharina A-E / Vasseur, Florence / Louedec, Liliane / Placier, Sandrine / Frère, Perrine / Verpont, Marie-Christine / Galichon, Pierre / Buob, David / Hadchouel, Juliette / Terzi, Fabiola / Chatziantoniou, Christos / Calmont, Amélie

The Journal of physiology

2024 Volume 602, Issue 8, Page(s) 1815–1833

Abstract: Renin is the key enzyme of the systemic renin-angiotensin-aldosterone system, which plays an essential role in regulating blood pressure and maintaining electrolyte and extracellular volume homeostasis. Renin is mainly produced and secreted by ... ...

Abstract	Renin is the key enzyme of the systemic renin-angiotensin-aldosterone system, which plays an essential role in regulating blood pressure and maintaining electrolyte and extracellular volume homeostasis. Renin is mainly produced and secreted by specialized juxtaglomerular (JG) cells in the kidney. In the present study, we report for the first time that the conserved transmembrane receptor neuropilin-1 (NRP1) participates in the development of JG cells and plays a key role in renin production. We used the myelin protein zero-Cre (P0-Cre) to abrogate Nrp1 constitutively in P0-Cre lineage-labelled cells of the kidney. We found that the P0-Cre precursor cells differentiate into renin-producing JG cells. We employed a lineage-tracing strategy combined with RNAscope quantification and metabolic studies to reveal a cell-autonomous role for NRP1 in JG cell function. Nrp1-deficient animals displayed abnormal levels of tissue renin expression and failed to adapt properly to a homeostatic challenge to sodium balance. These findings provide new insights into cell fate decisions and cellular plasticity operating in P0-Cre-expressing precursors and identify NRP1 as a novel key regulator of JG cell maturation. KEY POINTS: Renin is a centrepiece of the renin-angiotensin-aldosterone system and is produced by specialized juxtaglomerular cells (JG) of the kidney. Neuropilin-1 (NRP1) is a conserved membrane-bound receptor that regulates vascular and neuronal development, cancer aggressiveness and fibrosis progression. We used conditional mutagenesis and lineage tracing to show that NRP1 is expressed in JG cells where it regulates their function. Cell-specific Nrp1 knockout mice present with renin paucity in JG cells and struggle to adapt to a homeostatic challenge to sodium balance. The results support the versatility of renin-producing cells in the kidney and may open new avenues for therapeutic approaches.
MeSH term(s)	Mice ; Animals ; Renin/metabolism ; Juxtaglomerular Apparatus/metabolism ; Neuropilin-1/genetics ; Neuropilin-1/metabolism ; Kidney/metabolism ; Mice, Knockout ; Sodium/metabolism
Chemical Substances	Renin (EC 3.4.23.15) ; Neuropilin-1 (144713-63-3) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2024-02-21
Publishing country	England
Document type	Journal Article
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP285422
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Article ; Online: Heterozygous expression of Cre recombinase in podocytes has no impact on the anti-glomerular basement membrane glomerulonephritis model in C57BL/6J mice.

Mousseaux, Cyril / Migeon, Tiffany / Frère, Perrine / Verpont, Marie Christine / Lutete, Elisabeth / Navarro, Claire / Louedec, Liliane / Hadchouel, Juliette

Physiological reports

2022 Volume 10, Issue 17, Page(s) e15443

Abstract: A recent article described a thickening of the glomerular basement membrane (GBM) along with changes in the expression of key components of the extracellular matrix in 6-month-old NPHS2-Cre transgenic mice, which express the Cre recombinase specifically ... ...

Abstract	A recent article described a thickening of the glomerular basement membrane (GBM) along with changes in the expression of key components of the extracellular matrix in 6-month-old NPHS2-Cre transgenic mice, which express the Cre recombinase specifically in podocytes. This transgenic line has been widely used to characterize the implication of candidate genes in glomerular diseases in younger mice. Using a different mouse strain (C57BL/6J) than the previous report (129S6/SvEvTac), we sought to characterize 3- and 6-month-old NPHS2-Cre
MeSH term(s)	Animals ; Disease Models, Animal ; Glomerular Basement Membrane/metabolism ; Glomerulonephritis/metabolism ; Integrases/genetics ; Integrases/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Podocytes/metabolism
Chemical Substances	Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2022-09-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.15443
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Article ; Online: Recurrence of Anti-Semaphorin 3B-Mediated Membranous Nephropathy after Kidney Transplantation.

Fila, Marc / Debiec, Hanna / Perrochia, Hélène / Djouadi, Nabila / Verpont, Marie-Christine / Buob, David / Ronco, Pierre

Journal of the American Society of Nephrology : JASN

2022 Volume 33, Issue 3, Page(s) 503–509

Abstract: Background: Membranous nephropathy (MN) is rare in pediatric patients, although its diagnosis may be underestimated in children who are responsive to corticosteroid therapy prescribed for a suspicion of minimal change disease. It is most often ... ...

Abstract	Background: Membranous nephropathy (MN) is rare in pediatric patients, although its diagnosis may be underestimated in children who are responsive to corticosteroid therapy prescribed for a suspicion of minimal change disease. It is most often associated with an autoimmune disease, predominantly lupus. We previously reported the occurrence of early-onset MN associated with semaphorin 3B in nine children and two adults. Methods: Biopsies were performed on native kidney and at 1 and 5 months after transplantation. Semaphorin 3B antigen was detected in immune deposits by immunohistochemistry and confocal microscopy on paraffin-embedded biopsies. Anti-semaphorin antibodies were detected by Western blot and analyzed sequentially. Results: We report the first case of early recurrence after transplantation in a 7-year-old boy who presented with severe nephrotic syndrome and advanced kidney failure. There was no evidence of hereditary or associated autoimmune disease. Abundant, almost coalescent deposits were seen by electron microscopy and bright granular, subepithelial staining was observed for semaphorin 3B antigen. Western blot analysis of serum revealed anti-semaphorin 3B antibodies. Recurrence of MN occurred 25 days after transplantation and manifested as nephrotic range proteinuria despite conventional immunosuppressive therapy. Kidney biopsies confirmed histologic MN recurrence with colocalization of semaphorin 3B antigen and IgG. The patient was treated with rituximab. Anti-semaphorin 3B antibodies, which were detected at transplantation, were not detected 40 days after rituximab. Conclusion: This case provides evidence that anti-semaphorin 3B antibodies are pathogenic and should be monitored in patients with MN.
MeSH term(s)	Adult ; Autoimmune Diseases ; Child ; Female ; Glomerulonephritis, Membranous ; Humans ; Kidney Transplantation/adverse effects ; Male ; Receptors, Phospholipase A2 ; Recurrence ; Rituximab ; Semaphorins
Chemical Substances	Receptors, Phospholipase A2 ; Semaphorins ; Rituximab (4F4X42SYQ6)
Language	English
Publishing date	2022-01-11
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2021101323
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Article ; Online: Thrombospondin type-1 domain-containing 7A-related membranous nephropathy associated with glomerular AL amyloidosis.

Morel, Antoine / Buob, David / Goujon, Jean-Michel / Belhadj, Karim / Verpont, Marie-Christine / Audard, Vincent / Moktefi, Anissa

Pathology

2021 Volume 54, Issue 5, Page(s) 654–657

MeSH term(s)	Autoantibodies ; Glomerulonephritis, Membranous/complications ; Glomerulonephritis, Membranous/diagnosis ; Humans ; Immunoglobulin Light-chain Amyloidosis/complications ; Kidney Diseases ; Receptors, Phospholipase A2 ; Thrombospondins
Chemical Substances	Autoantibodies ; Receptors, Phospholipase A2 ; Thrombospondins
Language	English
Publishing date	2021-11-10
Publishing country	England
Document type	Letter
ZDB-ID	7085-3
ISSN	1465-3931 ; 0031-3025
ISSN (online)	1465-3931
ISSN	0031-3025
DOI	10.1016/j.pathol.2021.08.008
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Article ; Online: Protective Role of the Podocyte IL-15 / STAT5 Pathway in Focal Segmental Glomerulosclerosis.

Niasse, Aïssata / Louis, Kevin / Lenoir, Olivia / Schwarz, Chloé / Xu, Xiaoli / Couturier, Aymeric / Dobosziewicz, Hélène / Corchia, Anthony / Placier, Sandrine / Vandermeersch, Sophie / Hennighausen, Lothar / Frère, Perrine / Galichon, Pierre / Surin, Brigitte / Ouchelouche, Souhila / Louedec, Liliane / Migeon, Tiffany / Verpont, Marie-Christine / Yousfi, Nadir /

Buob, David / Xu-Dubois, Yi-Chun / François, Hélène / Rondeau, Eric / Mesnard, Laurent / Hadchouel, Juliette / Luque, Yosu

Kidney international reports

2024 Volume 9, Issue 4, Page(s) 1093–1106

Abstract: Introduction: During glomerular diseases, podocyte-specific pathways can modulate the intensity of histological disease and prognosis. The therapeutic targeting of these pathways could thus improve the management and prognosis of kidney diseases. The ... ...

Abstract	Introduction: During glomerular diseases, podocyte-specific pathways can modulate the intensity of histological disease and prognosis. The therapeutic targeting of these pathways could thus improve the management and prognosis of kidney diseases. The Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway, classically described in immune cells, has been recently described in detail in intrinsic kidney cells. Methods: We describe STAT5 expression in human kidney biopsies from patients with focal segmental glomerulosclerosis (FSGS) and studied mice with a podocyte-specific Results: Here, we show, for the first time, that STAT5 is activated in human podocytes in FSGS. In addition, podocyte-specific Conclusion: Activating podocyte STAT5 with commercially available IL-15 represents a potential new therapeutic avenue for FSGS.
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2024.01.010
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Article ; Online: Comparative therapeutic strategies for preventing aortic rupture in a mouse model of vascular Ehlers-Danlos syndrome.

Legrand, Anne / Guery, Charline / Faugeroux, Julie / Fontaine, Erika / Beugnon, Carole / Gianfermi, Amélie / Loisel-Ferreira, Irmine / Verpont, Marie-Christine / Adham, Salma / Mirault, Tristan / Hadchouel, Juliette / Jeunemaitre, Xavier

PLoS genetics

2022 Volume 18, Issue 3, Page(s) e1010059

Abstract: Vascular Ehlers-Danlos syndrome is a rare inherited disorder caused by genetic variants in type III collagen. Its prognosis is especially hampered by unpredictable arterial ruptures and there is no therapeutic consensus. We created a knock-in Col3a1+/ ... ...

Abstract	Vascular Ehlers-Danlos syndrome is a rare inherited disorder caused by genetic variants in type III collagen. Its prognosis is especially hampered by unpredictable arterial ruptures and there is no therapeutic consensus. We created a knock-in Col3a1+/G182R mouse model and performed a complete genetic, molecular and biochemical characterization. Several therapeutic strategies were also tested. Col3a1+/G182R mice showed a spontaneous mortality caused by thoracic aortic rupture that recapitulates the vascular Ehlers-Danlos syndrome with a lower survival rate in males, thin non-inflammatory arteries and an altered arterial collagen. Transcriptomic analysis of aortas showed upregulation of genes related to inflammation and cell stress response. Compared to water, survival rate of Col3a1+/G182R mice was not affected by beta-blockers (propranolol or celiprolol). Two other vasodilating anti-hypertensive agents (hydralazine, amlodipine) gave opposite results on aortic rupture and mortality rate. There was a spectacular beneficial effect of losartan, reversed by the cessation of its administration, and a marked deleterious effect of exogenous angiotensin II. These results suggest that blockade of the renin angiotensin system should be tested as a first-line medical therapy in patients with vascular Ehlers-Danlos syndrome.
MeSH term(s)	Animals ; Aortic Rupture/genetics ; Aortic Rupture/prevention & control ; Arteries ; Collagen Type III/genetics ; Disease Models, Animal ; Ehlers-Danlos Syndrome/drug therapy ; Ehlers-Danlos Syndrome/genetics ; Humans ; Male ; Mice
Chemical Substances	Collagen Type III
Language	English
Publishing date	2022-03-04
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1010059
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Article ; Online: Nanoscale Analysis of Randall's Plaques by Electron Energy Loss Spectromicroscopy: Insight in Early Biomineral Formation in Human Kidney.

Gay, Clément / Letavernier, Emmanuel / Verpont, Marie-Christine / Walls, Michael / Bazin, Dominique / Daudon, Michel / Nassif, Nadine / Stéphan, Odile / de Frutos, Marta

ACS nano

2020 Volume 14, Issue 2, Page(s) 1823–1836

Abstract: Idiopathic kidney stones originate mainly from calcium phosphate deposits at the tip of renal papillae, known as Randall's plaques (RPs), also detected in most human kidneys without stones. However, little is known about the mechanisms involved in RP ... ...

Abstract	Idiopathic kidney stones originate mainly from calcium phosphate deposits at the tip of renal papillae, known as Randall's plaques (RPs), also detected in most human kidneys without stones. However, little is known about the mechanisms involved in RP formation. The localization and characterization of such nanosized objects in the kidney remain a real challenge, making their study arduous. This study provides a nanoscale analysis of the chemical composition and morphology of incipient RPs, characterizing in particular the interface between the mineral and the surrounding organic compounds. Relying on data gathered from a calculi collection, the morphology and chemical composition of incipient calcifications in renal tissue were determined using spatially resolved electron energy-loss spectroscopy. We detected microcalcifications and individual nanocalcifications found at some distance from the larger ones. Strikingly, concerning the smaller ones, we show that two types of nanocalcifications coexist: calcified organic vesicles and nanometric mineral granules mainly composed of calcium phosphate with carbonate in their core. Interestingly, some of these nanocalcifications present similarities with those reported in physiological bone or pathological cardiovascular biominerals, suggesting possible common formation mechanisms. However, the high diversity of these nanocalcifications suggests that several mechanisms may be involved (nucleation on a carbonate core or on organic compounds). In addition, incipient RPs also appear to present specific features at larger scales, revealing secondary calcified structures embedded in a fibrillar organic material. Our study proves that analogies exist between physiological and pathological biominerals and provides information to understand the physicochemical processes involved in pathological calcification formation.
MeSH term(s)	Calcium Phosphates/analysis ; Calcium Phosphates/metabolism ; Electrons ; Humans ; Kidney Calculi/chemistry ; Kidney Calculi/diagnostic imaging ; Kidney Calculi/metabolism ; Kidney Medulla/chemistry ; Kidney Medulla/diagnostic imaging ; Kidney Medulla/metabolism ; Nanotechnology ; Particle Size ; Spectroscopy, Electron Energy-Loss ; Surface Properties
Chemical Substances	Calcium Phosphates ; calcium phosphate (97Z1WI3NDX)
Language	English
Publishing date	2020-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1936-086X
ISSN (online)	1936-086X
DOI	10.1021/acsnano.9b07664
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Article ; Online: Biallelic CAV1 null variants induce congenital generalized lipodystrophy with achalasia.

Karhan, Asuman Nur / Zammouri, Jamila / Auclair, Martine / Capel, Emilie / Apaydin, Feramuz Demir / Ates, Fehmi / Verpont, Marie-Christine / Magré, Jocelyne / Fève, Bruno / Lascols, Olivier / Usta, Yusuf / Jéru, Isabelle / Vigouroux, Corinne

European journal of endocrinology

2021 Volume 185, Issue 6, Page(s) 841–854

Abstract: Objective: CAV1 encodes caveolin-1, a major protein of plasma membrane microdomains called caveolae, involved in several signaling pathways. Caveolin-1 is also located at the adipocyte lipid droplet. Heterozygous pathogenic variants of CAV1 induce rare ... ...

Abstract	Objective: CAV1 encodes caveolin-1, a major protein of plasma membrane microdomains called caveolae, involved in several signaling pathways. Caveolin-1 is also located at the adipocyte lipid droplet. Heterozygous pathogenic variants of CAV1 induce rare heterogeneous disorders including pulmonary arterial hypertension and neonatal progeroid syndrome. Only one patient was previously reported with a CAV1 homozygous pathogenic variant, associated with congenital generalized lipodystrophy (CGL3). We aimed to further delineate genetic transmission, clinical, metabolic, and cellular characteristics of CGL3. Design/methods: In a large consanguineous kindred referred for CGL, we performed next-generation sequencing, as well as clinical, imagery, and metabolic investigations. We studied skin fibroblasts from the index case and the previously reported patient with CGL3. Results: Four patients, aged 8 months to 18 years, carried a new homozygous p.(His79Glnfs3) CAV1 variant. They all displayed generalized lipodystrophy since infancy, insulin resistance, low HDL-cholesterol, and/or high triglycerides, but no pulmonary hypertension. Two patients also presented at the age of 15 and 18 years with dysphagia due to achalasia, and one patient had retinitis pigmentosa. Heterozygous parents and relatives (n = 9) were asymptomatic, without any metabolic abnormality. Patients' fibroblasts showed a complete loss of caveolae and no protein expression of caveolin-1 and its caveolin-2 and cavin-1 partners. Patients' fibroblasts also displayed insulin resistance, increased oxidative stress, and premature senescence. Conclusions:* The CAV1 null variant investigated herein leads to an autosomal recessive congenital lipodystrophy syndrome. Loss of caveolin-1 and/or caveolae induces specific manifestations including achalasia which requires specific management. Overlapping phenotypic traits between the different CAV1-related diseases require further studies.
MeSH term(s)	Adolescent ; Caveolae/pathology ; Caveolae/ultrastructure ; Caveolin 1/genetics ; Caveolin 1/metabolism ; Caveolin 2/metabolism ; Cellular Senescence ; Child ; Child, Preschool ; Consanguinity ; Dyslipidemias/metabolism ; Esophageal Achalasia/genetics ; Esophageal Achalasia/pathology ; Female ; Fibroblasts/pathology ; Fibroblasts/ultrastructure ; Homozygote ; Humans ; Infant ; Lipodystrophy, Congenital Generalized/genetics ; Lipodystrophy, Congenital Generalized/metabolism ; Lipodystrophy, Congenital Generalized/pathology ; Male ; Microscopy, Electron, Transmission ; Oxidative Stress ; Pedigree ; RNA-Binding Proteins/metabolism
Chemical Substances	CAV1 protein, human ; CAV2 protein, human ; CAVIN1 protein, human ; Caveolin 1 ; Caveolin 2 ; RNA-Binding Proteins
Language	English
Publishing date	2021-11-10
Publishing country	England
Document type	Journal Article
ZDB-ID	1183856-5
ISSN	1479-683X ; 0804-4643
ISSN (online)	1479-683X
ISSN	0804-4643
DOI	10.1530/EJE-21-0915
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Article ; Online: Tubuloreticular inclusions in COVID-19-related collapsing glomerulopathy.

Gaillard, François / Ismael, Sophie / Sannier, Aurélie / Tarhini, Hassan / Volpe, Thomas / Greze, Clarisse / Verpont, Marie Christine / Zouhry, Ilyass / Rioux, Christophe / Lescure, François-Xavier / Buob, David / Daugas, Eric

Kidney international

2020 Volume 98, Issue 1, Page(s) 241

MeSH term(s)	Aged ; COVID-19 ; Coronavirus Infections/complications ; Coronavirus Infections/pathology ; Humans ; Inclusion Bodies/ultrastructure ; Kidney Diseases/pathology ; Kidney Diseases/virology ; Kidney Glomerulus/ultrastructure ; Male ; Pandemics ; Pneumonia, Viral/complications ; Pneumonia, Viral/pathology
Keywords	covid19
Language	English
Publishing date	2020-04-27
Publishing country	United States
Document type	Case Reports
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2020.04.022
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Article ; Online: Profile of an “at cutting edge” pathology laboratory for pathological human deposits

Bazin, Dominique / Lucas, Ivan T. / Rouzière, Stéphan / Elkaim, Erik / Mocuta, Cristian / Réguer, Solenn / Reid, David G. / Mathurin, Jérémie / Dazzi, Alexandre / Deniset-Besseau, Ariane / Petay, Margaux / Frochot, Vincent / Haymann, Jean-Philippe / Letavernier, Emmanuel / Verpont, Marie-Christine / Foy, Eddy / Bouderlique, Elise / Colboc, Hester / Daudon, Michel

Comptes Rendus. Chimie, Vol 25, Iss S1, Pp 219-

from nanometer to in vivo scale analysis on large scale facilities

2022 Volume 233

Abstract: This contribution aims to define an analysis procedure for abnormal deposits in human tissues starting from in vivo characterization, down to the nanoscale using major instrumentation. Such an integrated approach is based on recent literature, but ... ...

Abstract	This contribution aims to define an analysis procedure for abnormal deposits in human tissues starting from in vivo characterization, down to the nanoscale using major instrumentation. Such an integrated approach is based on recent literature, but particularly on our research over the last twenty years on pathological calcifications. To this end, we begin by describing four successive analytical steps, on the injury site or physician’s surgery, at the hospital, at a typical physicochemical laboratory, and finally at a large scale (possibly multinational) facility. For the first step, we present various techniques which can be implemented on portable instruments. For the second step, commercial analytical setups are used. In a physicochemical laboratory, prototype or commercial setups are used and finally on large scale instruments, characterization techniques with better spatial resolution and/or higher sensitivity or techniques specific to synchrotron radiation are employed.
Keywords	Pathological calcifications ; Characterization techniques ; Experimental approach ; Medical diagnostic ; Abnormal deposits ; Biochemistry ; QD415-436 ; Physical and theoretical chemistry ; QD450-801 ; Mathematics ; QA1-939
Language	English
Publishing date	2022-07-01T00:00:00Z
Publisher	Académie des sciences
Document type	Article ; Online
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