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Article ; Online: A comprehensive mouse kidney atlas enables rare cell population characterization and robust marker discovery.

Novella-Rausell, Claudio / Grudniewska, Magda / Peters, Dorien J M / Mahfouz, Ahmed

iScience

2023 Volume 26, Issue 6, Page(s) 106877

Abstract: The kidney's cellular diversity is on par with its physiological intricacy; yet identifying cell populations and their markers remains challenging. Here, we created a comprehensive atlas of the healthy adult mouse kidney (MKA: Mouse Kidney Atlas) by ... ...

Abstract	The kidney's cellular diversity is on par with its physiological intricacy; yet identifying cell populations and their markers remains challenging. Here, we created a comprehensive atlas of the healthy adult mouse kidney (MKA: Mouse Kidney Atlas) by integrating 140.000 cells and nuclei from 59 publicly available single-cell and single-nuclei RNA-sequencing datasets from eight independent studies. To harmonize annotations across datasets, we built a hierarchical model of the cell populations. Our model allows the incorporation of novel cell populations and the refinement of known profiles as more datasets become available. Using MKA and the learned model of cellular hierarchies, we predicted previously missing cell annotations from several studies. The MKA allowed us to identify reproducible markers across studies for poorly understood cell types and transitional states, which we verified using existing data from micro-dissected samples and spatial transcriptomics.
Language	English
Publishing date	2023-05-18
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106877
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Article ; Online: Molecular pathways involved in injury-repair and ADPKD progression.

Formica, Chiara / Peters, Dorien J M

Cellular signalling

2020 Volume 72, Page(s) 109648

Abstract: The major hallmark of Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the formation of many fluid-filled cysts in the kidneys, which ultimately impairs the normal renal structure and function, leading to end-stage renal disease (ESRD). A large ... ...

Abstract	The major hallmark of Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the formation of many fluid-filled cysts in the kidneys, which ultimately impairs the normal renal structure and function, leading to end-stage renal disease (ESRD). A large body of evidence suggests that injury-repair mechanisms are part of ADPKD progression. Once cysts have been formed, proliferation and fluid secretion contribute to the cyst size increase, which eventually causes stress on the surrounding tissue resulting in local injury and fibrosis. In addition, renal injury can cause or accelerate cyst formation. In this review, we will describe the various mechanisms activated during renal injury and tissue repair and show how they largely overlap with the molecular mechanisms activated during PKD progression. In particular, we will discuss molecular mechanisms such as proliferation, inflammation, cell differentiation, cytokines and growth factors secretion, which are activated following the renal injury to allow the remodelling of the tissue and a proper organ repair. We will also underline how, in a context of PKD-related gene mutations, aberrant or chronic activation of these developmental pathways and repair/remodelling mechanisms results in exacerbation of the disease.
MeSH term(s)	Animals ; Disease Progression ; Epigenesis, Genetic ; Humans ; Kidney/injuries ; Kidney/pathology ; Models, Biological ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/pathology ; Signal Transduction
Language	English
Publishing date	2020-04-19
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2020.109648
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Article ; Online: Inhibition of pannexin-1 does not restore electrolyte balance in precystic Pkd1 knockout mice.

van Megen, Wouter H / van Houtert, Teun J / Bos, Caro / Peters, Dorien J M / de Baaij, Jeroen H F / Hoenderop, Joost G J

Physiological reports

2024 Volume 12, Issue 7, Page(s) e15956

Abstract: Mutations in PKD1 and PKD2 cause autosomal dominant polycystic kidney disease (ADPKD), which is characterized by the formation of fluid-filled cysts in the kidney. In a subset of ADPKD patients, reduced blood calcium ( ... ...

Abstract	Mutations in PKD1 and PKD2 cause autosomal dominant polycystic kidney disease (ADPKD), which is characterized by the formation of fluid-filled cysts in the kidney. In a subset of ADPKD patients, reduced blood calcium (Ca
MeSH term(s)	Animals ; Humans ; Mice ; Adenosine Triphosphate/metabolism ; Kidney/metabolism ; Mice, Knockout ; Mutation ; Polycystic Kidney, Autosomal Dominant/metabolism ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism ; TRPP Cation Channels/pharmacology ; Water-Electrolyte Balance
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; TRPP Cation Channels ; polycystic kidney disease 1 protein ; Panx1 protein, mouse
Language	English
Publishing date	2024-04-01
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/phy2.15956
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Article ; Online: Transport and barrier mechanisms that regulate ciliary compartmentalization and ciliopathies.

Moran, Ailis L / Louzao-Martinez, Laura / Norris, Dominic P / Peters, Dorien J M / Blacque, Oliver E

Nature reviews. Nephrology

2023 Volume 20, Issue 2, Page(s) 83–100

Abstract: Primary cilia act as cell surface antennae, coordinating cellular responses to sensory inputs and signalling molecules that regulate developmental and homeostatic pathways. Cilia are therefore critical to physiological processes, and defects in ciliary ... ...

Abstract	Primary cilia act as cell surface antennae, coordinating cellular responses to sensory inputs and signalling molecules that regulate developmental and homeostatic pathways. Cilia are therefore critical to physiological processes, and defects in ciliary components are associated with a large group of inherited pleiotropic disorders - known collectively as ciliopathies - that have a broad spectrum of phenotypes and affect many or most tissues, including the kidney. A central feature of the cilium is its compartmentalized structure, which imparts its unique molecular composition and signalling environment despite its membrane and cytosol being contiguous with those of the cell. Such compartmentalization is achieved via active transport pathways that bring protein cargoes to and from the cilium, as well as gating pathways at the ciliary base that establish diffusion barriers to protein exchange into and out of the organelle. Many ciliopathy-linked proteins, including those involved in kidney development and homeostasis, are components of the compartmentalizing machinery. New insights into the major compartmentalizing pathways at the cilium, namely, ciliary gating, intraflagellar transport, lipidated protein flagellar transport and ciliary extracellular vesicle release pathways, have improved our understanding of the mechanisms that underpin ciliary disease and associated renal disorders.
MeSH term(s)	Humans ; Ciliopathies/metabolism ; Biological Transport ; Protein Transport ; Cilia/metabolism ; Cell Membrane/metabolism
Language	English
Publishing date	2023-10-23
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-023-00773-2
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Zs.A 6334: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: Preclinical evaluation of tolvaptan and salsalate combination therapy in a

Song, Xuewen / Leonhard, Wouter N / Kanhai, Anish A / Steinberg, Gregory R / Pei, York / Peters, Dorien J M

Frontiers in molecular biosciences

2023 Volume 10, Page(s) 1058825

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2023-01-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2023.1058825
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Article ; Online: Transcriptomic profiling of Polycystic Kidney Disease identifies paracrine factors in the early cyst microenvironment.

Yasinoglu, Sevtap A / Kuipers, Thomas B / Suidgeest, Ernst / van der Weerd, Louise / Mei, Hailiang / Baelde, Hans J / Peters, Dorien J M

Biochimica et biophysica acta. Molecular basis of disease

2023 Volume 1870, Issue 2, Page(s) 166987

Abstract: Initial cysts that are formed upon Pkd1 loss in mice impose persistent stress on surrounding tissue and trigger a cystic snowball effect, in which local aberrant PKD-related signaling increases the likelihood of new cyst formation, ultimately leading to ... ...

Abstract	Initial cysts that are formed upon Pkd1 loss in mice impose persistent stress on surrounding tissue and trigger a cystic snowball effect, in which local aberrant PKD-related signaling increases the likelihood of new cyst formation, ultimately leading to accelerated disease progression. Although many pathways have been associated with PKD progression, the knowledge of early changes near initial cysts is limited. To perform an unbiased analysis of transcriptomic alterations in the cyst microenvironment, microdomains were collected from kidney sections of iKsp-Pkd1
MeSH term(s)	Mice ; Animals ; Polycystic Kidney Diseases/genetics ; Polycystic Kidney Diseases/metabolism ; Kidney/metabolism ; Gene Expression Profiling ; Cysts/genetics ; Tumor Microenvironment
Language	English
Publishing date	2023-12-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2023.166987
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Article ; Online: Change in Urinary Myoinositol/Citrate Ratio Associates with Progressive Loss of Renal Function in ADPKD Patients.

Dekker, Shosha E I / Verhoeven, Aswin / Frey, Daria / Soonawala, Darius / Peters, Dorien J M / Mayboroda, Oleg A / de Fijter, Johan W

American journal of nephrology

2022 Volume 53, Issue 6, Page(s) 470–480

Abstract: Introduction: In autosomal dominant polycystic kidney disease (ADPKD) patients, predicting renal disease progression is important to make a prognosis and to support the clinical decision whether to initiate renoprotective therapy. Conventional markers ... ...

Abstract	Introduction: In autosomal dominant polycystic kidney disease (ADPKD) patients, predicting renal disease progression is important to make a prognosis and to support the clinical decision whether to initiate renoprotective therapy. Conventional markers all have their limitations. Metabolic profiling is a promising strategy for risk stratification. We determined the prognostic performance to identify patients with a fast progressive disease course and evaluated time-dependent changes in urinary metabolites. Methods: Targeted, quantitative metabolomics analysis (1H NMR-spectroscopy) was performed on spot urinary samples at two time points, baseline (n = 324, 61% female; mean age 45 years, SD 11; median eGFR 61 mL/min/1.73 m2, IQR 42-88; mean years of creatinine follow-up 3.7, SD 1.3) and a sample obtained after 3 years of follow-up (n = 112). Patients were stratified by their eGFR slope into fast and slow progressors based on an annualized change of > -3.0 or ≤ -3.0 mL/min/1.73 m2/year, respectively. Fifty-five urinary metabolites and ratios were quantified, and the significant ones were selected. Logistic regression was used to determine prognostic performance in identifying those with a fast progressive course using baseline urine samples. Repeated-measures ANOVA was used to analyze whether changes in urinary metabolites over a 3-year follow-up period differed between fast and slow progressors. Results: In a single urinary sample, the prognostic performance of urinary metabolites was comparable to that of a model including height-adjusted total kidney volume (htTKV, AUC = 0.67). Combined with htTKV, the predictive value of the metabolite model increased (AUC = 0.75). Longitudinal analyses showed an increase in the myoinositol/citrate ratio (p < 0.001) in fast progressors, while no significant change was found in those with slow progression, which is in-line with an overall increase in the myoinositol/citrate ratio as GFR declines. Conclusion: A metabolic profile, measured at a single time point, showed at least equivalent prognostic performance to an imaging-based risk marker in ADPKD. Changes in urinary metabolites over a 3-year follow-up period were associated with a fast progressive disease course.
MeSH term(s)	Citric Acid/metabolism ; Disease Progression ; Female ; Glomerular Filtration Rate ; Humans ; Inositol/metabolism ; Kidney ; Male ; Middle Aged ; Polycystic Kidney, Autosomal Dominant
Chemical Substances	Citric Acid (2968PHW8QP) ; Inositol (4L6452S749)
Language	English
Publishing date	2022-05-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604540-6
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000524851
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Article ; Online: Loss of function of renal Glut2 reverses hyperglycaemia and normalises body weight in mouse models of diabetes and obesity.

de Souza Cordeiro, Leticia Maria / Bainbridge, Lauren / Devisetty, Nagavardhini / McDougal, David H / Peters, Dorien J M / Chhabra, Kavaljit H

Diabetologia

2022 Volume 65, Issue 6, Page(s) 1032–1047

Abstract: Aims/hypothesis: Renal GLUT2 is increased in diabetes, thereby enhancing glucose reabsorption and worsening hyperglycaemia. Here, we determined whether loss of Glut2 (also known as Slc2a2) specifically in the kidneys would reverse hyperglycaemia and ... ...

Abstract	Aims/hypothesis: Renal GLUT2 is increased in diabetes, thereby enhancing glucose reabsorption and worsening hyperglycaemia. Here, we determined whether loss of Glut2 (also known as Slc2a2) specifically in the kidneys would reverse hyperglycaemia and normalise body weight in mouse models of diabetes and obesity. Methods: We used the tamoxifen-inducible CreERT2-Lox system in mice to knockout Glut2 specifically in the kidneys (Ks-Glut2 KO) to establish the contribution of renal GLUT2 to systemic glucose homeostasis in health and in insulin-dependent as well as non-insulin-dependent diabetes. We measured circulating glucose and insulin levels in response to OGTT or IVGTT under different experimental conditions in the Ks-Glut2 KO and their control mice. Moreover, we quantified urine glucose levels to explain the phenotype of the mice independently of insulin actions. We also used a transcription factor array to identify mechanisms underlying the crosstalk between renal GLUT2 and sodium-glucose cotransporter 2 (SGLT2). Results: The Ks-Glut2 KO mice exhibited improved glucose tolerance and massive glucosuria. Interestingly, this improvement in blood glucose control was eliminated when we knocked out Glut2 in the liver in addition to the kidneys, suggesting that the improvement is attributable to the lack of renal GLUT2. Remarkably, induction of renal Glut2 deficiency reversed hyperglycaemia and normalised body weight in mouse models of diabetes and obesity. Longitudinal monitoring of renal glucose transporters revealed that Sglt2 (also known as Slc5a2) expression was almost abolished 3 weeks after inducing renal Glut2 deficiency. To identify a molecular basis for this crosstalk, we screened for renal transcription factors that were downregulated in the Ks-Glut2 KO mice. Hnf1α (also known as Hnf1a) was among the genes most downregulated and its recovery restored Sglt2 expression in primary renal proximal tubular cells isolated from the Ks-Glut2 KO mice. Conclusions/interpretation: Altogether, these results demonstrate a novel crosstalk between renal GLUT2 and SGLT2 in regulating systemic glucose homeostasis via glucose reabsorption. Our findings also indicate that inhibiting renal GLUT2 is a potential therapy for diabetes and obesity.
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Disease Models, Animal ; Female ; Glucose/metabolism ; Glucose Transporter Type 2 ; Glycosuria/metabolism ; Humans ; Hyperglycemia/metabolism ; Insulin/metabolism ; Kidney/metabolism ; Male ; Mice ; Obesity/genetics ; Obesity/metabolism ; Sodium-Glucose Transporter 2/genetics ; Sodium-Glucose Transporter 2/metabolism
Chemical Substances	Blood Glucose ; Glucose Transporter Type 2 ; Insulin ; Slc2a2 protein, mouse ; Sodium-Glucose Transporter 2 ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-03-15
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-022-05676-8
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Article ; Online: Translational research in ADPKD: lessons from animal models.

Happé, Hester / Peters, Dorien J M

Nature reviews. Nephrology

2014 Volume 10, Issue 10, Page(s) 587–601

Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 or PKD2, which encode polycystin-1 and polycystin-2, respectively. Rodent models are available to study the pathogenesis of polycystic kidney disease (PKD) and for ... ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 or PKD2, which encode polycystin-1 and polycystin-2, respectively. Rodent models are available to study the pathogenesis of polycystic kidney disease (PKD) and for preclinical testing of potential therapies-either genetically engineered models carrying mutations in Pkd1 or Pkd2 or models of renal cystic disease that do not have mutations in these genes. The models are characterized by age at onset of disease, rate of disease progression, the affected nephron segment, the number of affected nephrons, synchronized or unsynchronized cyst formation and the extent of fibrosis and inflammation. Mouse models have provided valuable mechanistic insights into the pathogenesis of PKD; for example, mutated Pkd1 or Pkd2 cause renal cysts but additional factors are also required, and the rate of cyst formation is increased in the presence of renal injury. Animal studies have also revealed complex genetic and functional interactions among various genes and proteins associated with PKD. Here, we provide an update on the preclinical models commonly used to study the molecular pathogenesis of ADPKD and test potential therapeutic strategies. Progress made in understanding the pathophysiology of human ADPKD through these animal models is also discussed.
MeSH term(s)	Animals ; Disease Models, Animal ; Disease Progression ; Gene Dosage ; Gene Expression ; Mice ; Mutation ; Polycystic Kidney, Autosomal Dominant/genetics ; TRPP Cation Channels/genetics
Chemical Substances	TRPP Cation Channels ; polycystic kidney disease 1 protein ; polycystic kidney disease 2 protein
Language	English
Publishing date	2014-08-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2014.137
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Article ; Online: Extracellular vesicles contribute to early cyst development in autosomal dominant polycystic kidney disease by cell-to-cell communication.

Carotti, Valentina / van Megen, Wouter H / Rigalli, Juan P / Barros, Eric R / Sommers, Vera / Rutten, Luco / Sommerdijk, Nico / Peters, Dorien J M / van Asbeck-van der Wijst, Jenny / Hoenderop, Joost G J

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 7, Page(s) e23006

Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of fluid-filled cysts within the kidney due to mutations in PKD1 or PKD2. Although the disease remains incompletely understood, one of the factors associated with ... ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of fluid-filled cysts within the kidney due to mutations in PKD1 or PKD2. Although the disease remains incompletely understood, one of the factors associated with ADPKD progression is the release of nucleotides (including ATP), which can initiate autocrine or paracrine purinergic signaling by binding to their receptors. Recently, we and others have shown that increased extracellular vesicle (EVs) release from PKD1 knockout cells can stimulate cyst growth through effects on recipient cells. Given that EVs are an important communicator between different nephron segments, we hypothesize that EVs released from PKD1 knockout distal convoluted tubule (DCT) cells can stimulate cyst growth in the downstream collecting duct (CD). Here, we show that administration of EVs derived from Pkd1
MeSH term(s)	Mice ; Animals ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/metabolism ; Kidney/metabolism ; Cell Communication ; Extracellular Vesicles/metabolism ; Adenosine Triphosphate/metabolism ; Cysts/metabolism ; TRPP Cation Channels/metabolism
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; TRPP Cation Channels
Language	English
Publishing date	2023-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202300490R
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