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Article ; Online: Assessing Urinary Tract Junction Obstruction Defects by Methylene Blue Dye Injection.

Yun, Kangsun

Journal of visualized experiments : JoVE

2017 , Issue 128

Abstract: Urinary tract junction obstruction defects are congenital anomalies inducing hydronephrosis and hydroureter. Murine urinary tract junction obstruction defects can be assessed by tracking methylene blue dye flow within the urinary system. Methylene blue ... ...

Abstract	Urinary tract junction obstruction defects are congenital anomalies inducing hydronephrosis and hydroureter. Murine urinary tract junction obstruction defects can be assessed by tracking methylene blue dye flow within the urinary system. Methylene blue dye is injected into the renal pelvis of perinatal embryonic kidneys and dye flow is monitored from the renal pelvis of the kidney through the ureter and into the bladder lumen after applying hydrostatic pressure. Dye accumulation will be evident in the bladder lumen of the normal perinatal urinary tract, but will be constrained between the renal pelvis and the end point of an abnormal ureter, if urinary tract obstructions occur. This method facilitates the confirmation of urinary tract junction obstructions and visualization of hydronephrosis and hydroureter. This manuscript describes a protocol for methylene blue dye injection into the renal pelvis to confirm urinary tract junction obstructions.
MeSH term(s)	Humans ; Hydronephrosis/diagnosis ; Methylene Blue/therapeutic use ; Urinary Tract/pathology
Chemical Substances	Methylene Blue (T42P99266K)
Language	English
Publishing date	2017-10-12
Publishing country	United States
Document type	Journal Article ; Video-Audio Media ; Research Support, N.I.H., Extramural
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/56247
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Assessing urinary tract junction obstruction defects by methylene blue dye injection

Yun, Kangsun

Journal of visualized experiments. 2017 Oct. 12, , no. 128

2017

Abstract	Urinary tract junction obstruction defects are congenital anomalies inducing hydronephrosis and hydroureter. Murine urinary tract junction obstruction defects can be assessed by tracking methylene blue dye flow within the urinary system. Methylene blue dye is injected into the renal pelvis of perinatal embryonic kidneys and dye flow is monitored from the renal pelvis of the kidney through the ureter and into the bladder lumen after applying hydrostatic pressure. Dye accumulation will be evident in the bladder lumen of the normal perinatal urinary tract, but will be constrained between the renal pelvis and the end point of an abnormal ureter, if urinary tract obstructions occur. This method facilitates the confirmation of urinary tract junction obstructions and visualization of hydronephrosis and hydroureter. This manuscript describes a protocol for methylene blue dye injection into the renal pelvis to confirm urinary tract junction obstructions.
Keywords	bladder ; congenital abnormalities ; hydrostatic pressure ; kidneys ; methylene blue ; mice ; pelvis ; ureter
Language	English
Dates of publication	2017-1012
Size	p. e56247.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/56247
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Article ; Online: Constitutive metanephric mesenchyme-specific expression of interferon-gamma causes renal dysplasia by regulating Sall1 expression.

Kangsun Yun / Arthur A Hurwitz / Alan O Perantoni

PLoS ONE, Vol 13, Iss 5, p e

2018 Volume 0197356

Abstract: Transplacental viral and parasitic infections have been shown to initiate an innate response in the mammalian embryo by increasing the expression of pro-inflammatory cytokines such as interferon-gamma (Ifng). However, the developmental consequences of an ...

Abstract	Transplacental viral and parasitic infections have been shown to initiate an innate response in the mammalian embryo by increasing the expression of pro-inflammatory cytokines such as interferon-gamma (Ifng). However, the developmental consequences of an activated innate immunity and, in particular, the effects of induction of Ifng expression independent of infection have been largely overlooked. Here, we demonstrate in vivo that the conditional overexpression of Ifng in metanephric mesenchymal (MM) progenitors results in renal agenesis or hypoplasia. Cell death was observed in and around the MM region of E10.5-11.5 mutants where Ifng was constitutively expressed during early kidney development and resulted in a retardation of branching morphogenesis. Furthermore, isolated mutant or normal Ifng-treated metanephroi replicated this phenotype in culture, demonstrating the inherent nature of the aberrant morphogenesis. The expression of renal progenitor marker Sall1 was significantly decreased in the MM of mutant kidneys, suggesting that a reduction in Sall1 may be the cause of cell death in the MM during early kidney development and that, in turn, retards UB branching in the mutants. Therefore, the aberrant induction of Ifng expression, as part of an innate immune response, may contribute to renal agenesis or hypoplasia during early metanephric development by regulating the MM progenitor population.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2018-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Hydronephrosis in the Wnt5a-ablated kidney is caused by an abnormal ureter-bladder connection.

Yun, Kangsun / Perantoni, Alan O

Differentiation; research in biological diversity

2016 Volume 94, Page(s) 1–7

Abstract: The Wnt5a null mouse is a complex developmental model which, among its several posterior-localized axis defects, exhibits multiple kidney phenotypes, including duplex kidney and loss of the medullary zone. We previously reported that ablation of Wnt5a in ...

Abstract	The Wnt5a null mouse is a complex developmental model which, among its several posterior-localized axis defects, exhibits multiple kidney phenotypes, including duplex kidney and loss of the medullary zone. We previously reported that ablation of Wnt5a in nascent mesoderm causes duplex kidney formation as a result of aberrant development of the nephric duct and abnormal extension of intermediate mesoderm. However, these mice also display a loss of the medullary region late in gestation. We have now genetically isolated duplex kidney formation from the medullary defect by specifically targeting the progenitors for both the ureteric bud and metanephric mesenchyme. The conditional mutants fail to form a normal renal medulla but no longer exhibit duplex kidney formation. Approximately 1/3 of the mutants develop hydronephrosis in the kidneys either uni- or bilaterally when using Dll1Cre. The abnormal kidney phenotype becomes prominent at E16.5, which approximates the time when urine production begins in the mouse embryonic kidney, and is associated with a dramatic increase in apoptosis only in mutant kidneys with hydronephrosis. Methylene blue dye injection and histologic examination reveal that aberrant cell death likely results from urine toxicity due to an abnormal ureter-bladder connection. This study shows that Wnt5a is not required for development of the renal medulla and that loss of the renal medullary region in the Wnt5a-deleted kidney is caused by an abnormal ureter-bladder connection.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Hydronephrosis/genetics ; Hydronephrosis/physiopathology ; Kidney/growth & development ; Kidney/physiopathology ; Mice ; Mice, Knockout ; Morphogenesis/genetics ; Signal Transduction/genetics ; Ureter/abnormalities ; Ureter/growth & development ; Urinary Bladder/abnormalities ; Urinary Bladder/growth & development ; Wnt-5a Protein/genetics
Chemical Substances	Wnt-5a Protein
Language	English
Publishing date	2016-12-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2016.11.006
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Zs.A 1170: Show issues

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Article ; Online: Constitutive metanephric mesenchyme-specific expression of interferon-gamma causes renal dysplasia by regulating Sall1 expression.

Yun, Kangsun / Hurwitz, Arthur A / Perantoni, Alan O

PloS one

2018 Volume 13, Issue 5, Page(s) e0197356

Abstract	Transplacental viral and parasitic infections have been shown to initiate an innate response in the mammalian embryo by increasing the expression of pro-inflammatory cytokines such as interferon-gamma (Ifng). However, the developmental consequences of an activated innate immunity and, in particular, the effects of induction of Ifng expression independent of infection have been largely overlooked. Here, we demonstrate in vivo that the conditional overexpression of Ifng in metanephric mesenchymal (MM) progenitors results in renal agenesis or hypoplasia. Cell death was observed in and around the MM region of E10.5-11.5 mutants where Ifng was constitutively expressed during early kidney development and resulted in a retardation of branching morphogenesis. Furthermore, isolated mutant or normal Ifng-treated metanephroi replicated this phenotype in culture, demonstrating the inherent nature of the aberrant morphogenesis. The expression of renal progenitor marker Sall1 was significantly decreased in the MM of mutant kidneys, suggesting that a reduction in Sall1 may be the cause of cell death in the MM during early kidney development and that, in turn, retards UB branching in the mutants. Therefore, the aberrant induction of Ifng expression, as part of an innate immune response, may contribute to renal agenesis or hypoplasia during early metanephric development by regulating the MM progenitor population.
MeSH term(s)	Animals ; Cell Death/physiology ; Gene Expression Regulation, Developmental ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Kidney/abnormalities ; Kidney/embryology ; Kidney/metabolism ; Mesenchymal Stem Cells/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Organogenesis/physiology ; Tissue Culture Techniques ; Transcription Factors/metabolism
Chemical Substances	IFNG protein, mouse ; Sall1 protein, mouse ; Transcription Factors ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2018-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0197356
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Transcriptional regulation of MMP13 by Lef1 in chondrocytes.

Yun, Kangsun / Im, Sin-Hyeog

Biochemical and biophysical research communications

2007 Volume 364, Issue 4, Page(s) 1009–1014

Abstract: An association between Wnt/beta-catenin signaling and MMP13 expression has been reported but there has been little information about the underlying mechanism. Here, we investigated the role of Lef1 in IL-1beta-mediated MMP13 regulation in mouse ... ...

Abstract	An association between Wnt/beta-catenin signaling and MMP13 expression has been reported but there has been little information about the underlying mechanism. Here, we investigated the role of Lef1 in IL-1beta-mediated MMP13 regulation in mouse chondrocytes. Lef1 and beta-catenin synergistically upregulated MMP13 transcription while knock-down of Lef1 using Lef1 siRNA downregulated IL-1beta-mediated MMP13 expression. Lef1 binding site was mapped to the 3' region of the MMP13 genomic locus and binding of Lef1/beta-catenin to the site was confirmed by chromatin immunoprecipitation (ChIP) assays and electrophoretic mobility shift assays (EMSAs). Furthermore, Lef1/beta-catenin binding to the Lef1 binding site transactivated MMP13 promoter activity. Our results suggest a pivotal role of Lef1/beta-catenin in MMP13 regulation in chondrocytes, which might be associated with matrix loss of degenerated arthritic cartilage.
MeSH term(s)	Animals ; Cells, Cultured ; Chondrocytes/metabolism ; Gene Expression Regulation/physiology ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Matrix Metalloproteinase 13/metabolism ; Mice ; Transcriptional Activation/physiology
Chemical Substances	Lef1 protein, mouse ; Lymphoid Enhancer-Binding Factor 1 ; Matrix Metalloproteinase 13 (EC 3.4.24.-) ; Mmp13 protein, mouse (EC 3.4.24.-)
Language	English
Publishing date	2007-12-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2007.10.121
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Zs.A 116: Show issues

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Article ; Online: Lef1 regulates COX-2 transcription in chondrocytes.

Yun, Kangsun / Im, Sin-Hyeog

Biochemical and biophysical research communications

2007 Volume 364, Issue 2, Page(s) 270–275

Abstract: Although the involvement of Wnt/beta-catenin signaling pathway in the regulation of COX-2 expression has been suggested, the underlying molecular mechanisms are still unclear. Here, we demonstrate that lymphoid enhancer-binding factor 1 (Lef1) in concert ...

Abstract	Although the involvement of Wnt/beta-catenin signaling pathway in the regulation of COX-2 expression has been suggested, the underlying molecular mechanisms are still unclear. Here, we demonstrate that lymphoid enhancer-binding factor 1 (Lef1) in concert with beta-catenin is associated with the transcriptional regulation of the gene encoding COX-2 in mouse chondrocytes. Our results show that co-overexpression of Lef1 and beta-catenin synergistically upregulates COX-2 expression. Furthermore, decrease of Lef1 expression using Lef1 siRNA results in the downregulation of COX-2 expression. Using bioinformatic analysis, we identified a conserved Lef1-binding site that is mapped at the 3' region of the genomic COX-2 locus. In vivo and in vitro binding of Lef1 at the predicted binding site was proved using chromatin immunoprecipitation assays and electrophoretic mobility shift assays, respectively. Moreover, binding of Lef1 and beta-catenin to the Lef1-binding site transactivates COX-2 promoter activity. Our results indicate a pivotal role of Lef1 in the regulation of COX-2 transcription in arthritic chondrocytes.
MeSH term(s)	Animals ; Binding Sites ; Cells, Cultured ; Chondrocytes/metabolism ; Computational Biology ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/physiology ; Electrophoretic Mobility Shift Assay ; Gene Expression Regulation ; Immunoprecipitation ; Lymphoid Enhancer-Binding Factor 1/genetics ; Lymphoid Enhancer-Binding Factor 1/physiology ; Mice ; Mice, Inbred ICR ; Promoter Regions, Genetic ; Transcription, Genetic ; Transcriptional Activation ; beta Catenin/metabolism
Chemical Substances	Lef1 protein, mouse ; Lymphoid Enhancer-Binding Factor 1 ; beta Catenin ; Ptgs2 protein, mouse (EC 1.14.99.-) ; Cyclooxygenase 2 (EC 1.14.99.1)
Language	English
Publishing date	2007-12-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2007.09.129
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Article ; Online: Looping mediated interaction between the promoter and 3' UTR regulates type II collagen expression in chondrocytes.

Arijita Jash / Kangsun Yun / Anupama Sahoo / Jae-Seon So / Sin-Hyeog Im

PLoS ONE, Vol 7, Iss 7, p e

2012 Volume 40828

Abstract: Type II collagen is the major component of articular cartilage and is mainly synthesized by chondrocytes. Repeated sub-culturing of primary chondrocytes leads to reduction of type II collagen gene (Col2a1) expression, which mimics the process of ... ...

Abstract	Type II collagen is the major component of articular cartilage and is mainly synthesized by chondrocytes. Repeated sub-culturing of primary chondrocytes leads to reduction of type II collagen gene (Col2a1) expression, which mimics the process of chondrocyte dedifferentiation. Although the functional importance of Col2a1 expression has been extensively investigated, mechanism of transcriptional regulation during chondrocyte dedifferentiation is still unclear. In this study, we have investigated the crosstalk between cis-acting DNA element and transcription factor on Col2a1 expression in primary chondrocytes. Bioinformatic analysis revealed the potential regulatory regions in the Col2a1 genomic locus. Among them, promoter and 3' untranslated region (UTR) showed highly accessible chromatin architecture with enriched recruitment of active chromatin markers in primary chondrocytes. 3' UTR has a potent enhancer function which recruits Lef1 (Lymphoid enhancer binding factor 1) transcription factor, leading to juxtaposition of the 3' UTR with the promoter through gene looping resulting in up-regulation of Col2a1 gene transcription. Knock-down of endogenous Lef1 level significantly reduced the gene looping and subsequently down-regulated Col2a1 expression. However, these regulatory loci become inaccessible due to condensed chromatin architecture as chondrocytes dedifferentiate which was accompanied by a reduction of gene looping and down-regulation of Col2a1 expression. Our results indicate that Lef1 mediated looping between promoter and 3' UTR under the permissive chromatin architecture upregulates Col2a1 expression in primary chondrocytes.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Looping mediated interaction between the promoter and 3' UTR regulates type II collagen expression in chondrocytes.

Jash, Arijita / Yun, Kangsun / Sahoo, Anupama / So, Jae-Seon / Im, Sin-Hyeog

PloS one

2012 Volume 7, Issue 7, Page(s) e40828

Abstract	Type II collagen is the major component of articular cartilage and is mainly synthesized by chondrocytes. Repeated sub-culturing of primary chondrocytes leads to reduction of type II collagen gene (Col2a1) expression, which mimics the process of chondrocyte dedifferentiation. Although the functional importance of Col2a1 expression has been extensively investigated, mechanism of transcriptional regulation during chondrocyte dedifferentiation is still unclear. In this study, we have investigated the crosstalk between cis-acting DNA element and transcription factor on Col2a1 expression in primary chondrocytes. Bioinformatic analysis revealed the potential regulatory regions in the Col2a1 genomic locus. Among them, promoter and 3' untranslated region (UTR) showed highly accessible chromatin architecture with enriched recruitment of active chromatin markers in primary chondrocytes. 3' UTR has a potent enhancer function which recruits Lef1 (Lymphoid enhancer binding factor 1) transcription factor, leading to juxtaposition of the 3' UTR with the promoter through gene looping resulting in up-regulation of Col2a1 gene transcription. Knock-down of endogenous Lef1 level significantly reduced the gene looping and subsequently down-regulated Col2a1 expression. However, these regulatory loci become inaccessible due to condensed chromatin architecture as chondrocytes dedifferentiate which was accompanied by a reduction of gene looping and down-regulation of Col2a1 expression. Our results indicate that Lef1 mediated looping between promoter and 3' UTR under the permissive chromatin architecture upregulates Col2a1 expression in primary chondrocytes.
MeSH term(s)	3' Untranslated Regions/genetics ; Animals ; Cell Dedifferentiation/genetics ; Cells, Cultured ; Chondrocytes/cytology ; Chondrocytes/metabolism ; Chromatin/metabolism ; Collagen Type II/genetics ; Collagen Type II/metabolism ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic ; Gene Expression Regulation ; Genetic Loci/genetics ; Humans ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Mice ; Mice, Inbred ICR ; Nucleic Acid Conformation ; Promoter Regions, Genetic ; Protein Binding/genetics ; Transcription, Genetic ; Up-Regulation/genetics
Chemical Substances	3' Untranslated Regions ; Chromatin ; Col2a1 protein, mouse ; Collagen Type II ; Lef1 protein, mouse ; Lymphoid Enhancer-Binding Factor 1
Language	English
Publishing date	2012-07-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0040828
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Non-canonical Wnt5a/Ror2 signaling regulates kidney morphogenesis by controlling intermediate mesoderm extension.

Yun, Kangsun / Ajima, Rieko / Sharma, Nirmala / Costantini, Frank / Mackem, Susan / Lewandoski, Mark / Yamaguchi, Terry P / Perantoni, Alan O

Human molecular genetics

2014 Volume 23, Issue 25, Page(s) 6807–6814

Abstract: Congenital anomalies of the kidney and urinary tract (CAKUT) affect about 1 in 500 births and are a major cause of morbidity in infants. Duplex collecting systems rank among the most common abnormalities of CAKUT, but the molecular basis for this defect ... ...

Abstract	Congenital anomalies of the kidney and urinary tract (CAKUT) affect about 1 in 500 births and are a major cause of morbidity in infants. Duplex collecting systems rank among the most common abnormalities of CAKUT, but the molecular basis for this defect is poorly understood. In mice, conditional deletion of Wnt5a in mesoderm results in bilateral duplex kidney and ureter formation. The ureteric buds (UBs) in mutants emerge as doublets from the intermediate mesoderm (IM)-derived nephric duct (ND) without anterior expansion of the glial cell line-derived neurotrophic factor (Gdnf) expression domain in the surrounding mesenchyme. Wnt5a is normally expressed in a graded manner at the posterior end of the IM, but its expression is down-regulated prior to UB outgrowth at E10.5. Furthermore, ablation of Wnt5a in the mesoderm with an inducible Cre at E7.5 results in duplex UBs, whereas ablation at E8.5 yields normal UB outgrowth, demonstrating that Wnt5a functions in IM development well before the formation of the metanephros. In mutants, the posterior ND is duplicated and surrounding Pax2-positive mesenchymal cells persist in the nephric cord, suggesting that disruption of normal ND patterning prompts the formation of duplex ureters and kidneys. Ror2 homozygous mutants, which infrequently yield duplex collecting systems, show a dramatic increase in incidence with the additional deletion of one copy of Wnt5a, implicating this receptor in non-canonical Wnt5a signaling during IM development. This work provides the first evidence of a role of Wnt5a/Ror2 signaling in IM extension and offers new insights into the etiology of CAKUT and possible involvement of Wnt5a/Ror2 mutations.
MeSH term(s)	Animals ; Embryo, Mammalian ; Gene Expression Regulation, Developmental ; Glial Cell Line-Derived Neurotrophic Factor/genetics ; Glial Cell Line-Derived Neurotrophic Factor/metabolism ; Homozygote ; Integrases/genetics ; Integrases/metabolism ; Kidney/growth & development ; Kidney/metabolism ; Kidney/pathology ; Mesenchymal Stem Cells/metabolism ; Mesenchymal Stem Cells/pathology ; Mesoderm/growth & development ; Mesoderm/metabolism ; Mesoderm/pathology ; Mice ; Mice, Transgenic ; Morphogenesis/genetics ; PAX2 Transcription Factor/genetics ; PAX2 Transcription Factor/metabolism ; Receptor Tyrosine Kinase-like Orphan Receptors/genetics ; Receptor Tyrosine Kinase-like Orphan Receptors/metabolism ; Signal Transduction/genetics ; Time Factors ; Ureter/growth & development ; Ureter/metabolism ; Ureter/pathology ; Wnt Proteins/deficiency ; Wnt Proteins/genetics ; Wnt-5a Protein ; Wolffian Ducts/growth & development ; Wolffian Ducts/metabolism ; Wolffian Ducts/pathology
Chemical Substances	Glial Cell Line-Derived Neurotrophic Factor ; PAX2 Transcription Factor ; Pax2 protein, mouse ; Wnt Proteins ; Wnt-5a Protein ; Wnt5a protein, mouse ; Receptor Tyrosine Kinase-like Orphan Receptors (EC 2.7.10.1) ; Ror2 protein, mouse (EC 2.7.10.1) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2014-07-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddu397
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