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  1. Article ; Online: Deletion of the prorenin receptor in the ureteric bud in mice inhibits Dot1/H3K79 pathway.

    Song, Renfang / Yosypiv, Ihor V

    Pediatric research

    2024  

    Abstract: Background: The prorenin receptor (PRR) plays a critical role in ureteric bud (UB) branching morphogenesis. DOT1 Like (DOT1L), a histone methyltransferase specific for Histone 3 lysine 79 (H3K79), is important for differentiation of the UB-derived renal ...

    Abstract Background: The prorenin receptor (PRR) plays a critical role in ureteric bud (UB) branching morphogenesis. DOT1 Like (DOT1L), a histone methyltransferase specific for Histone 3 lysine 79 (H3K79), is important for differentiation of the UB-derived renal collecting duct cells. In this study, we tested whether DOT1L/H3 dimethyl K79 (H3m2K79) are regulated by PRR deletion in the UB and UB-derived collecting ducts in the embryonic mouse kidneys.
    Methods: Mutant Hoxb7
    Results: DOT1L mRNA levels were decreased in mutant compared to control mice (0.68 ± 0.06 vs. 1.0 ± 0.01, p < 0.01). DOT1L and H3m2K79 immunostaining was reduced in the mutant vs. control kidneys (Dot1: 0.62 ± 0.03 vs. 1.0 ± 0.01, p < 0.05; H3m2K79: 0.64 ± 0.04 vs.1.1 ± 0.01. p < 0.05.). Western blot analysis revealed decreased H3m2K79 protein levels in mutant compared to control kidneys (1.0 ± 0.06 vs. 1.5 ± 0.02, p < 0.05).
    Conclusion: Targeted deletion of the PRR in the UB and UB-derived collecting ducts results in reduced DOT1L gene/protein and H3m2K79 protein expression in the embryonic mouse metanephroi in vivo.
    Impact: The role of histone methylation in mediating the effect of the prorenin receptor on the ureteric bud branching (UB) morphogenesis and urine acidification during kidney development is unknown. We demonstrate that histone H3 lysine (K) 79 dimethylation by methyltransferase Dot1 is reduced in the embryonic kidney of mice that lack the prorenin receptor in the UB lineage.
    Language English
    Publishing date 2024-01-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 4411-8
    ISSN 1530-0447 ; 0031-3998
    ISSN (online) 1530-0447
    ISSN 0031-3998
    DOI 10.1038/s41390-024-03026-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Nephrotic Syndrome in a Child With

    Tollaksen, Ross / Craver, Randall D / Yosypiv, Ihor V

    Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society

    2024  , Page(s) 10935266231223274

    Abstract: Steroid resistant nephrotic syndrome (SRNS) accounts for 30% of all cases of nephrotic syndrome (NS) in children and frequently leads to end stage kidney disease (ESKD). About 30% of children with SRNS demonstrate causative mutations in podocyte- ... ...

    Abstract Steroid resistant nephrotic syndrome (SRNS) accounts for 30% of all cases of nephrotic syndrome (NS) in children and frequently leads to end stage kidney disease (ESKD). About 30% of children with SRNS demonstrate causative mutations in podocyte- associated genes. Early identification of genetic forms of SRNS is critical to avoid potentially harmful immunosuppressive therapy. A 2-year-old male patient with NS and no family history of renal disease did not respond to 4-week steroid treatment. Kidney biopsy demonstrated mesangial proliferative glomerulopathy with basement membrane dysmorphism. Tacrolimus and Lisinopril were added to therapy pending results of genetic testing. Kidney Gene panel showed a NPHS2 c.413G>A (p.Arg138Gln) homozygous pathogenic variant. This missense variant is considered a common pathogenic founder mutation in European populations. A diagnosis of autosomal-recessive form of nonsyndromic SRNS due to NPHS2 causative variant was made. Immunosuppresive therapy was stopped, Lizinopril dose was increased and weekly infusions of Albumin/furosemide were initiated to manage edema. This case demonstrates that early genetic testing in children with SRNS avoids prolonged potentially harmful immunosuppressive therapy, allows for timely genetic family counseling, and allows earlier consideration for future living related donor kidney transplantation.
    Language English
    Publishing date 2024-01-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1463498-3
    ISSN 1615-5742 ; 1093-5266
    ISSN (online) 1615-5742
    ISSN 1093-5266
    DOI 10.1177/10935266231223274
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  3. Article ; Online: Renin-angiotensin system in mammalian kidney development.

    Yosypiv, Ihor V

    Pediatric nephrology (Berlin, Germany)

    2020  Volume 36, Issue 3, Page(s) 479–489

    Abstract: Mutations in the genes of the renin-angiotensin system result in congenital anomalies of the kidney and urinary tract (CAKUT), the main cause of end-stage renal disease in children. The molecular mechanisms that cause CAKUT are unclear in most cases. To ... ...

    Abstract Mutations in the genes of the renin-angiotensin system result in congenital anomalies of the kidney and urinary tract (CAKUT), the main cause of end-stage renal disease in children. The molecular mechanisms that cause CAKUT are unclear in most cases. To improve the care of children with CAKUT, it is critical to determine the underlying mechanisms of CAKUT. In this review, we discuss recent advances that have helped to better understand how disruption of the renin-angiotensin system during kidney development contributes to CAKUT.
    MeSH term(s) Animals ; Humans ; Kidney ; Kidney Diseases ; Renin-Angiotensin System ; Urogenital Abnormalities ; Vesico-Ureteral Reflux
    Language English
    Publishing date 2020-02-18
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-020-04496-5
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  4. Article ; Online: Prorenin receptor in kidney development.

    Yosypiv, Ihor V

    Pediatric nephrology (Berlin, Germany)

    2017  Volume 32, Issue 3, Page(s) 383–392

    Abstract: Prorenin receptor (PRR), a receptor for renin and prorenin and an accessory subunit of the vacuolar proton pump ... ...

    Abstract Prorenin receptor (PRR), a receptor for renin and prorenin and an accessory subunit of the vacuolar proton pump H
    MeSH term(s) Animals ; Child ; Humans ; Kidney/growth & development ; Kidney/metabolism ; Kidney Diseases/genetics ; Kidney Diseases/metabolism ; Mice ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Vacuolar Proton-Translocating ATPases/genetics ; Vacuolar Proton-Translocating ATPases/metabolism
    Chemical Substances ATP6AP2 protein, human ; Receptors, Cell Surface ; prorenin receptor ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
    Language English
    Publishing date 2017
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-016-3365-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Sequence variants in the renin-angiotensin system genes are associated with isolated multicystic dysplastic kidney in children.

    Song, Renfang / Yosypiv, Ihor V

    Pediatric research

    2020  Volume 90, Issue 1, Page(s) 205–211

    Abstract: Background: Multicystic dysplastic kidney (MCDK) is a common form of congenital cystic kidney disease in children. The etiology of MCDK remains unclear. Given an important role of the renin-angiotensin system in normal kidney development, we explored ... ...

    Abstract Background: Multicystic dysplastic kidney (MCDK) is a common form of congenital cystic kidney disease in children. The etiology of MCDK remains unclear. Given an important role of the renin-angiotensin system in normal kidney development, we explored whether MCDK in children is associated with variants in the genes encoding renin-angiotensin system components by Sanger sequencing.
    Methods: The coding regions of renin (REN), angiotensinogen (AGT), ACE, and angiotensin 1 receptor (AGTR1) genes were amplified by PCR. The effect of DNA sequence variants on protein function was predicted with PolyPhen-2 software.
    Results: 3 novel and known AGT variants were found. 1 variant was probably damaging, 1 was possibly damaging and one was benign. Out of 7 REN variants, 4 were probably damaging and 3 were benign. Of 6 ACE variants, 3 were probably damaging and 3-benign. 3 AGTR1 variants were found. 2 variants were possibly damaging, and one was benign.
    Conclusion: We report novel associations of sequence variants in REN, AGT, ACE, or AGTR1 genes in children with isolated MCDK in the United States. Our findings suggest a recessive disease model and support the hypothesis of multiple renin-angiotensin system gene involvement in MCDK.
    Impact: Discovery of novel gene variants in renin-angiotensin genes in children with MCDK. Novel possibly damaging gene variants discovered. Multiple renin-angiotensin system gene variants are involved in MCDK.
    MeSH term(s) Angiotensinogen/genetics ; Case-Control Studies ; Child ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Multicystic Dysplastic Kidney/genetics ; Peptidyl-Dipeptidase A/genetics ; Receptor, Angiotensin, Type 1/genetics ; Renin/genetics ; Renin-Angiotensin System/genetics
    Chemical Substances AGT protein, human ; AGTR1 protein, human ; Receptor, Angiotensin, Type 1 ; Angiotensinogen (11002-13-4) ; ACE protein, human (EC 3.4.15.1) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Renin (EC 3.4.23.15)
    Language English
    Publishing date 2020-11-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 4411-8
    ISSN 1530-0447 ; 0031-3998
    ISSN (online) 1530-0447
    ISSN 0031-3998
    DOI 10.1038/s41390-020-01255-y
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  6. Article ; Online: Cytogenomic aberrations in isolated multicystic dysplastic kidney in children.

    Chen, Tian-Jian / Song, Renfang / Janssen, Adam / Yosypiv, Ihor V

    Pediatric research

    2021  Volume 91, Issue 3, Page(s) 659–664

    Abstract: Background: Multicystic dysplastic kidney (MCDK) is a common form of congenital kidney anomaly. The cause of MCDK is unknown. We investigated whether MCDK in children is linked to cytogenomic aberrations.: Methods: We conducted array comparative ... ...

    Abstract Background: Multicystic dysplastic kidney (MCDK) is a common form of congenital kidney anomaly. The cause of MCDK is unknown. We investigated whether MCDK in children is linked to cytogenomic aberrations.
    Methods: We conducted array comparative genomic hybridization (aCGH) in ten unrelated children with MCDK. The pattern of inheritance was determined by real-time PCR in patients and their biological parents.
    Results: Pathogenic aberrations were detected in three patients: a deletion at 7p14.3 with a size of 2.07 Mb housing 12 genes, including BBS9 (Bardet-Biedl syndrome 9) and BMPER (BMP binding endothelial regulator); a duplication at 16p13.11p12.3 with a size of 3.28 Mb that included >20 genes; and monosomy X for a female patient. The deletion at 7p14.3 was inherited from the patient's father, while the duplication at 16p13.11p12.3 was derived from the patient's mother.
    Conclusions: Up to 30% of patients with MCDK possess cytogenomic aberrations. BBS9 and BMPER variants have been reported to result in cystic kidney dysplasia, suggesting a possible pathogenic function for the deletion at 7p14.3 in children with MCDK. The duplication at 16p13.11p12.3 was not reported previously to associate with MCDK. Both variations were inherited from parents, indicating hereditary contributions in MCDK. Thus, aCGH is an informative tool to unravel the pathogenic mechanisms of MCDK.
    Impact: Cytogenomic aberrations are common in children with MCDK. Cytogenomic aberrations are inherited from parents, indicating hereditary contributions in MCDK. aCGH is a valuable tool to reveal pathogenic mechanisms of MCDK.
    MeSH term(s) Bardet-Biedl Syndrome/pathology ; Carrier Proteins/genetics ; Child ; Comparative Genomic Hybridization ; Female ; Humans ; Kidney/pathology ; Multicystic Dysplastic Kidney/genetics ; Multicystic Dysplastic Kidney/pathology
    Chemical Substances BMPER protein, human ; Carrier Proteins
    Language English
    Publishing date 2021-03-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 4411-8
    ISSN 1530-0447 ; 0031-3998
    ISSN (online) 1530-0447
    ISSN 0031-3998
    DOI 10.1038/s41390-021-01476-9
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  7. Article ; Online: Classic Bartter Syndrome: A Cause of Severe Hypokalemic Metabolic Alkalosis.

    Thakore, Poonam / Anderson, Margot / Yosypiv, Ihor V

    Clinical pediatrics

    2019  Volume 58, Issue 14, Page(s) 1557–1561

    MeSH term(s) Alkalosis/etiology ; Bartter Syndrome/diagnosis ; Bartter Syndrome/genetics ; Bartter Syndrome/metabolism ; Female ; Humans ; Hypokalemia/etiology ; Infant ; Sodium Chloride Symporters/metabolism
    Chemical Substances Sodium Chloride Symporters
    Language English
    Publishing date 2019-06-22
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 207678-0
    ISSN 1938-2707 ; 0009-9228
    ISSN (online) 1938-2707
    ISSN 0009-9228
    DOI 10.1177/0009922819857535
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  8. Article ; Online: Renin-angiotensin system in ureteric bud branching morphogenesis: implications for kidney disease.

    Yosypiv, Ihor V

    Pediatric nephrology (Berlin, Germany)

    2013  Volume 29, Issue 4, Page(s) 609–620

    Abstract: Failure of normal branching morphogenesis of the ureteric bud (UB), a key ontogenic process that controls organogenesis of the metanephric kidney, leads to congenital anomalies of the kidney and urinary tract (CAKUT), the leading cause of end-stage ... ...

    Abstract Failure of normal branching morphogenesis of the ureteric bud (UB), a key ontogenic process that controls organogenesis of the metanephric kidney, leads to congenital anomalies of the kidney and urinary tract (CAKUT), the leading cause of end-stage kidney disease in children. Recent studies have revealed a central role of the renin-angiotensin system (RAS), the cardinal regulator of blood pressure and fluid/electrolyte homeostasis, in the control of normal kidney development. Mice or humans with mutations in the RAS genes exhibit a spectrum of CAKUT which includes renal medullary hypoplasia, hydronephrosis, renal hypodysplasia, duplicated renal collecting system and renal tubular dysgenesis. Emerging evidence indicates that severe hypoplasia of the inner medulla and papilla observed in angiotensinogen (Agt)- or angiotensin (Ang) II AT 1 receptor (AT 1 R)-deficient mice is due to aberrant UB branching morphogenesis resulting from disrupted RAS signaling. Lack of the prorenin receptor (PRR) in the UB in mice causes reduced UB branching, resulting in decreased nephron endowment, marked kidney hypoplasia, urinary concentrating and acidification defects. This review provides a mechanistic rational supporting the hypothesis that aberrant signaling of the intrarenal RAS during distinct stages of metanephric kidney development contributes to the pathogenesis of the broad phenotypic spectrum of CAKUT. As aberrant RAS signaling impairs normal renal development, these findings advocate caution for the use of RAS inhibitors in early infancy and further underscore a need to avoid their use during pregnancy and to identify the types of molecular processes that can be targeted for clinical intervention.
    MeSH term(s) Animals ; Humans ; Kidney/embryology ; Kidney Diseases/congenital ; Kidney Diseases/metabolism ; Morphogenesis ; Renin-Angiotensin System/physiology ; Ureter/embryology ; Urogenital Abnormalities/metabolism
    Language English
    Publishing date 2013-09-07
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-013-2616-3
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  9. Article ; Online: Congenital anomalies of the kidney and urinary tract: a genetic disorder?

    Yosypiv, Ihor V

    International journal of nephrology

    2012  Volume 2012, Page(s) 909083

    Abstract: Congenital anomalies of the kidney and urinary tract (CAKUTs) occur in 3-6 per 1000 live births, account for the most cases of pediatric end-stage kidney disease (ESKD), and predispose an individual to hypertension and cardiovascular disease throughout ... ...

    Abstract Congenital anomalies of the kidney and urinary tract (CAKUTs) occur in 3-6 per 1000 live births, account for the most cases of pediatric end-stage kidney disease (ESKD), and predispose an individual to hypertension and cardiovascular disease throughout life. Although CAKUTs are a part of many known syndromes, only few single-candidate causative genes have been implicated so far in nonsyndromic cases of human CAKUT. Evidence from mouse models supports the hypothesis that non-syndromic human CAKUT may be caused by single-gene defects. Because increasing numbers of children with CAKUT are surviving to adulthood, better understanding of the molecular pathogenesis of CAKUT, development of new strategies aiming at prevention of CAKUT, preservation of renal function, and avoidance of associated cardiovascular morbidity are needed. In this paper, we will focus on the knowledge derived from the study of syndromic and non-syndromic forms of CAKUT in humans and mouse mutants to discuss the role of genetic, epigenetic, and in utero environmental factors in the pathogenesis of non-syndromic forms of CAKUT in children with particular emphasis on the genetic contributions to CAKUT.
    Language English
    Publishing date 2012-05-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2573904-9
    ISSN 2090-2158 ; 2090-214X
    ISSN (online) 2090-2158
    ISSN 2090-214X
    DOI 10.1155/2012/909083
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  10. Article ; Online: Renin-angiotensin system in ureteric bud branching morphogenesis: insights into the mechanisms.

    Yosypiv, Ihor V

    Pediatric nephrology (Berlin, Germany)

    2011  Volume 26, Issue 9, Page(s) 1499–1512

    Abstract: Branching morphogenesis of the ureteric bud (UB) is a key developmental process that controls organogenesis of the entire metanephros. Notably, aberrant UB branching may result in a spectrum of congenital anomalies of the kidney and urinary tract (CAKUT). ...

    Abstract Branching morphogenesis of the ureteric bud (UB) is a key developmental process that controls organogenesis of the entire metanephros. Notably, aberrant UB branching may result in a spectrum of congenital anomalies of the kidney and urinary tract (CAKUT). Genetic, biochemical and physiological studies have demonstrated that the renin-angiotensin system (RAS), a key regulator of the blood pressure and fluid/electrolyte homeostasis, also plays a critical role in kidney development. All the components of the RAS are expressed in the metanephros. Moreover, mutations in the genes encoding components of the RAS in mice or humans cause diverse types of CAKUT which include renal papillary hypoplasia, hydronephrosis, duplicated collecting system, renal tubular dysgenesis, renal vascular abnormalities, abnormal glomerulogenesis and urinary concentrating defect. Despite widely accepted role of the RAS in metanephric kidney and renal collecting system (ureter, pelvis, calyces and collecting ducts) development, the mechanisms by which an intact RAS exerts its morphogenetic actions are incompletely defined. Emerging evidence indicates that defects in UB branching morphogenesis may be causally linked to the pathogenesis of renal collecting system anomalies observed under conditions of aberrant RAS signaling. This review describes the role of the RAS in UB branching morphogenesis and highlights emerging insights into the cellular and molecular mechanisms whereby RAS regulates this critical morphogenetic process.
    MeSH term(s) Animals ; Gene Expression Regulation, Developmental ; Humans ; Morphogenesis ; Renin-Angiotensin System/genetics ; Signal Transduction/genetics ; Ureter/embryology ; Ureter/metabolism
    Language English
    Publishing date 2011-02-26
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-011-1820-2
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