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Article ; Online: Epigenetics and the control of the collecting duct epithelial sodium channel.

Kone, Bruce C

2013 Volume 33, Issue 4, Page(s) 383–391

Abstract: The apical membrane epithelial Na(+) channel subunit (ENaC) in series with the basolateral Na(+)/K(+)-adenosine triphosphatase mediates collecting duct Na(+) reabsorption. Aldosterone induces αENaC gene transcription, which appears to be rate limiting ... ...

Abstract	The apical membrane epithelial Na(+) channel subunit (ENaC) in series with the basolateral Na(+)/K(+)-adenosine triphosphatase mediates collecting duct Na(+) reabsorption. Aldosterone induces αENaC gene transcription, which appears to be rate limiting for ENaC activity in this segment. Although this response has long been assumed to be solely the result of liganded nuclear hormone receptors trans-activating αENaC, epigenetic controls of basal and aldosterone-induced transcription of αENaC in the collecting duct recently were described. These epigenetic pathways involve dynamic nuclear repressor complexes targeted to specific subregions of the αENaC promoter and consisting of the histone methyltransferase disrupter of telomeric silencing (Dot)1a together with the transcriptional factor Af9 or the nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase Sirt1, key co-regulatory proteins, including serum- and glucocorticoid-induced kinase-1 and the putative transcription factor Af17, and targeted chromatin modifications. The complexes, through the action of Dot1a, maintain chromatin associated with the αENaC promoter in a stable hypermethylated state, constraining αENaC transcription under basal conditions. Aldosterone and serum- and glucocorticoid-induced kinase-1, itself, activate αENaC transcription in large part by disrupting or diminishing the Dot1a-Af9 and Dot1a-Sirt1 complexes and their effects on chromatin. Mouse models indicate potential roles of the Dot1a pathways in renal salt excretion and hypertension.
MeSH term(s)	Aldosterone/physiology ; Animals ; Blood Pressure ; Epigenesis, Genetic ; Epithelial Sodium Channels/genetics ; Epithelial Sodium Channels/physiology ; Histone-Lysine N-Methyltransferase ; Humans ; Kidney Tubules, Collecting/metabolism ; Methyltransferases/physiology ; Promoter Regions, Genetic ; Sirtuin 1/physiology
Chemical Substances	Epithelial Sodium Channels ; Aldosterone (4964P6T9RB) ; DOT1L protein, human (EC 2.1.1.-) ; Methyltransferases (EC 2.1.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2013-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2013.05.010
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Article ; Online: A different perspective on admission decisions.

Kone, Bruce C

Academic medicine : journal of the Association of American Medical Colleges

2009 Volume 84, Issue 3, Page(s) 289; author reply 289

MeSH term(s)	Confidentiality ; Education, Medical, Undergraduate ; Humans ; School Admission Criteria ; United States
Language	English
Publishing date	2009-03
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	96192-9
ISSN	1938-808X ; 1040-2446
ISSN (online)	1938-808X
ISSN	1040-2446
DOI	10.1097/ACM.0b013e3181971ea5
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Article: 2009 Southern Society For Clinical Investigation presidential address: opportunity knocks.

Kone, Bruce C

The American journal of the medical sciences

2009 Volume 338, Issue 1, Page(s) 1–2

MeSH term(s)	Biomedical Research/economics ; Biomedical Research/standards ; Education, Medical ; Humans ; Societies, Medical
Language	English
Publishing date	2009-07
Publishing country	United States
Document type	Addresses
ZDB-ID	82078-7
ISSN	1538-2990 ; 0002-9629
ISSN (online)	1538-2990
ISSN	0002-9629
DOI	10.1097/MAJ.0b013e3181a86196
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Article: Lingo: an automated, web-based deep phenotyping platform for language ability.

Casten, Lucas G / Koomar, Tanner / Elsadany, Muhammad / McKone, Caleb / Tysseling, Ben / Sasidharan, Mahesh / Tomblin, J Bruce / Michaelson, Jacob J

medRxiv : the preprint server for health sciences

2024

Abstract: Background: Language and the ability to communicate effectively are key factors in mental health and well-being. Despite this critical importance, research on language is limited by the lack of a scalable phenotyping toolkit.: Methods: Here, we ... ...

Abstract	Background: Language and the ability to communicate effectively are key factors in mental health and well-being. Despite this critical importance, research on language is limited by the lack of a scalable phenotyping toolkit. Methods: Here, we describe and showcase Lingo - a flexible online battery of language and nonverbal reasoning skills based on seven widely used tasks (COWAT, picture narration, vocal rhythm entrainment, rapid automatized naming, following directions, sentence repetition, and nonverbal reasoning). The current version of Lingo takes approximately 30 minutes to complete, is entirely open source, and allows for a wide variety of performance metrics to be extracted. We asked > 1,300 individuals from multiple samples to complete Lingo, then investigated the validity and utility of the resulting data. Results: We conducted an exploratory factor analysis across 14 features derived from the seven assessments, identifying five factors. Four of the five factors showed acceptable test-retest reliability (Pearson's R > 0.7). Factor 2 showed the highest reliability (Pearson's R = 0.95) and loaded primarily on sentence repetition task performance. We validated Lingo with objective measures of language ability by comparing performance to gold-standard assessments: CELF-5 and the VABS-3. Factor 2 was significantly associated with the CELF-5 "core language ability" scale (Pearson's R = 0.77, p-value < 0.05) and the VABS-3 "communication" scale (Pearson's R = 0.74, p-value < 0.05). Factor 2 was positively associated with phenotypic and genetic measures of socieconomic status. Interestingly, we found the parents of children with language impairments had lower Factor 2 scores (p-value < 0.01). Finally, we found Lingo factor scores were significantly predictive of numerous psychiatric and neurodevelopmental conditions. Conclusions: Together, these analyses support Lingo as a powerful platform for scalable deep phenotyping of language and other cognitive abilities. Additionally, exploratory analyses provide supporting evidence for the heritability of language ability and the complex relationship between mental health and language.
Language	English
Publishing date	2024-03-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.29.24305034
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Article ; Online: NO break-ins at water gate.

Kone, Bruce C

Hypertension (Dallas, Tex. : 1979)

2006 Volume 48, Issue 1, Page(s) 29–30

MeSH term(s)	Aquaporin 1/metabolism ; Biological Transport ; Cell Membrane/metabolism ; Diffusion ; Humans ; Nitric Oxide/metabolism ; Permeability ; Water/metabolism
Chemical Substances	Water (059QF0KO0R) ; Aquaporin 1 (146410-94-8) ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/01.HYP.0000223653.56526.ed
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Article: Nitric oxide synthesis in the kidney: isoforms, biosynthesis, and functions in health.

Kone, Bruce C

Seminars in nephrology

2004 Volume 24, Issue 4, Page(s) 299–315

Abstract: Nitric oxide (NO) is a gaseous free radical that serves cell signaling, cellular energetics, host defense, and inflammatory functions in virtually all cells. In the kidney and vasculature, NO plays fundamental roles in the control of systemic and ... ...

Abstract	Nitric oxide (NO) is a gaseous free radical that serves cell signaling, cellular energetics, host defense, and inflammatory functions in virtually all cells. In the kidney and vasculature, NO plays fundamental roles in the control of systemic and intrarenal hemodynamics, the tubuloglomerular feedback response, pressure natriuresis, release of sympathetic neurotransmitters and renin, and tubular solute and water transport. NO is synthesized from L-arginine by NO synthases (NOS). Because of its high chemical reactivity and high diffusibility, NO production by each of the 3 major NOS isoforms is regulated tightly at multiple levels from gene transcription to spatial proximity near intended targets to covalent modification and allosteric regulation of the enzyme itself. Many of these regulatory mechanisms have yet to be tested in renal cells. The NOS isoforms are distributed differentially and regulated in the kidney, and there remains some controversy over the specific expression of functional protein for the NOS isoforms in specific renal cell populations. Mice with targeted deletion of each of the NOS isoforms have been generated, and these each have unique phenotypes. Studies of the renal and vascular phenotypes of these mice have yielded important insights into certain vascular diseases, ischemic acute renal failure, the tubuloglomerular feedback response, and some mechanisms of tubular fluid and electrolyte transport, but thus far have been underexploited. This review explores the collective knowledge regarding the structure, regulation, and function of the NOS isoforms gleaned from various tissues, and highlights the progress and gaps in understanding in applying this information to renal and vascular physiology.
MeSH term(s)	Animals ; Glomerular Filtration Rate ; Hemodynamics/physiology ; Homeostasis ; Humans ; Mice ; Mice, Knockout ; Natriuresis/physiology ; Nitric Oxide/biosynthesis ; Nitric Oxide Synthase/metabolism ; Protein Isoforms/biosynthesis ; Rats ; Rats, Inbred Dahl ; Reference Values ; Renal Circulation/physiology ; Structure-Activity Relationship
Chemical Substances	Protein Isoforms ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39)
Language	English
Publishing date	2004-07-13
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2004.04.002
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Article ; Online: Physical and functional interaction of Rnf2 with Af9 regulates basal and aldosterone-stimulated transcription of the α-ENaC gene in a renal collecting duct cell line.

Yu, Zhi-Yuan / Kong, Qun / Kone, Bruce C

Bioscience reports

2013 Volume 33, Issue 5

Abstract: The physical and functional interaction of Rnf2 (RING finger protein 2), a central component of the PRC (Polycomb repressive complex) 1 and Af9 (ALL1-fused gene from chromosome 9 protein), an aldosterone-sensitive transcription factor, in regulating ... ...

Abstract	The physical and functional interaction of Rnf2 (RING finger protein 2), a central component of the PRC (Polycomb repressive complex) 1 and Af9 (ALL1-fused gene from chromosome 9 protein), an aldosterone-sensitive transcription factor, in regulating basal and aldosterone-stimulated transcription of the α-ENaC (epithelial Na+ channel α-subunit) gene was explored in mIMCD3 CD (collecting duct) cells. Since Rnf2 lacks DNA-specific binding activity, other factors must mediate its site-specific chromatin recruitment. Rnf2 and Af9 co-localized in the nucleus and co-immunoprecipitated. A GST (glutathione transferase)-Af9 carboxy-terminal fusion protein directly interacted with in vitro translated Rnf2 in GST pull-down assays. Rnf2 knock down enhanced basal and aldosterone-stimulated α-ENaC mRNA levels and α-ENaC promoter activity. ChIP/QPCR (chromatin immunoprecipitation/quantitative PCR) assays demonstrated enrichment of Rnf2, H2AK119 (mono-ubiquitinated histone H2A lysine 119), and H3K27me3 (histone H3 lysine 27 trimethylated), a PRC2 chromatin mark, at multiple α-ENaC promoter subregions corresponding to regions of known Af9 enrichment, under basal conditions. Sequential ChIP confirmed Rnf2-Af9 co-occupancy of the α-ENaC promoter. Aldosterone provoked early and sustained depletion of Rnf2, ubiquitinated H2AK119, and trimethylated H3K27 associated with the subregions of the α-ENaC promoter. Thus, Af9 mediates site-selective physical and functional recruitment of Rnf2 to the α-ENaC promoter to constrain basal α-ENaC transcription in collecting duct cells, and aldosterone reverses this process.
MeSH term(s)	Aldosterone/physiology ; Animals ; Cell Line ; Epithelial Sodium Channels/genetics ; Epithelial Sodium Channels/metabolism ; Gene Expression Regulation ; Kidney Tubules, Collecting/cytology ; Mice ; Nuclear Proteins/chemistry ; Nuclear Proteins/metabolism ; Polycomb Repressive Complex 1/chemistry ; Polycomb Repressive Complex 1/metabolism ; Promoter Regions, Genetic ; Protein Binding ; Protein Interaction Mapping ; Protein Transport ; Transcription, Genetic ; Ubiquitin-Protein Ligases/chemistry ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Epithelial Sodium Channels ; Mllt3 protein, mouse ; Nuclear Proteins ; Aldosterone (4964P6T9RB) ; Polycomb Repressive Complex 1 (EC 2.3.2.27) ; Rnf2 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2013-10-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	764946-0
ISSN	1573-4935 ; 0144-8463
ISSN (online)	1573-4935
ISSN	0144-8463
DOI	10.1042/BSR20130086
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Article ; Online: Sp1 trans-activates and is required for maximal aldosterone induction of the αENaC gene in collecting duct cells.

Yu, Zhiyuan / Kong, Qun / Kone, Bruce C

American journal of physiology. Renal physiology

2013 Volume 305, Issue 5, Page(s) F653–62

Abstract: The epithelial Na+ channel (ENaC) in the distal nephron constitutes the rate-limiting step for renal sodium reabsorption. Aldosterone increases tubular sodium absorption in large part by increasing αENaC transcription in collecting duct principal cells. ... ...

Abstract	The epithelial Na+ channel (ENaC) in the distal nephron constitutes the rate-limiting step for renal sodium reabsorption. Aldosterone increases tubular sodium absorption in large part by increasing αENaC transcription in collecting duct principal cells. We previously reported that Af9 binds to +78/+92 of αENaC and recruits Dot1a to repress basal and aldosterone-sensitive αENaC transcription in mouse inner medullary collecting duct (mIMCD)3 cells. Despite this epigenetic repression, basal αENaC transcription is still evident and physiologically necessary, indicating basal operation of positive regulators. In the present study, we identified Sp1 as one such regulator. Gel shift and antibody competition assays using a +208/+240 probe revealed DNA-Sp1-containing complexes in mIMCD3 cells. Mutation of the +222/+229 element abrogated Sp1 binding in vitro and in promoter-reporter constructs stably expressed in mIMCD3 cells. Compared with the wild-type promoter, an αENaC promoter-luciferase construct with +222/+229 mutations exhibited much lower activity and impaired trans-activation in Sp1 overexpression experiments. Conversely, Sp1 knockdown inhibited endogenous αENaC mRNA and the activity of the wild-type αENaC promoter but not the mutated construct. Aldosterone triggered Sp1 recruitment to the αENaC promoter, which was required for maximal induction of αENaC promoter activity and was blocked by spironolactone. Sequential chromatin immunoprecipitation assays and functional tests of +78/+92 and +222/+229 αENaC promoter mutants indicated that while Sp1, Dot1a, and Af9 co-occupy the αENaC promoter, the Sp1 effects are functionally independent from Dot1a and Af9. In summary, Sp1 binding to a cis-element at +222/+229 represents the first identified constitutive driver of αENaC transcription, and it contributes to maximal aldosterone trans-activation of αENaC.
MeSH term(s)	Aldosterone/pharmacology ; Animals ; Cells, Cultured ; Epigenesis, Genetic/physiology ; Epithelial Sodium Channels/drug effects ; Epithelial Sodium Channels/genetics ; Epithelial Sodium Channels/metabolism ; Kidney Tubules, Collecting/cytology ; Mice ; Promoter Regions, Genetic/drug effects ; Sp1 Transcription Factor/metabolism ; Sp1 Transcription Factor/physiology ; Trans-Activators/pharmacology ; Transcription, Genetic/drug effects
Chemical Substances	Epithelial Sodium Channels ; Scnn1a protein, mouse ; Sp1 Transcription Factor ; Trans-Activators ; Aldosterone (4964P6T9RB)
Language	English
Publishing date	2013-06-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00177.2013
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Article ; Online: Aldosterone reprograms promoter methylation to regulate αENaC transcription in the collecting duct.

Yu, Zhiyuan / Kong, Qun / Kone, Bruce C

American journal of physiology. Renal physiology

2013 Volume 305, Issue 7, Page(s) F1006–13

Abstract: Aldosterone increases tubular Na(+) absorption largely by increasing α-epithelial Na(+) channel (αENaC) transcription in collecting duct principal cells. How aldosterone reprograms basal αENaC transcription to high-level activity in the collecting duct ... ...

Abstract	Aldosterone increases tubular Na(+) absorption largely by increasing α-epithelial Na(+) channel (αENaC) transcription in collecting duct principal cells. How aldosterone reprograms basal αENaC transcription to high-level activity in the collecting duct is incompletely understood. Promoter methylation, a covalent but reversible epigenetic process, has been implicated in the control of gene expression in health and disease. We investigated the role of promoter methylation/demethylation in the epigenetic control of basal and aldosterone-stimulated αENaC transcription in mIMCD3 collecting duct cells. Bisulfite treatment and sequencing analysis after treatment of the cells with the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (5-Aza-CdR) identified clusters of methylated cytosines in a CpG island near the transcription start site of the αENaC promoter. 5-Aza-CdR treatment or small interfering RNA-mediated knockdown of DNMT3b or methyl-CpG-binding domain protein (MBD)-4 derepressed basal αENaC transcription, indicating that promoter methylation suppresses basal αENaC transcription. Aldosterone triggered a time-dependent decrease in 5mC and DNMT3b and a concurrent enrichment in 5-hydroxymethylcytosine (5hmC) and ten-eleven translocation (Tet)2 at the αENaC promoter, consistent with active demethylation. 5-Aza-CdR mimicked aldosterone by enhancing Sp1 binding to the αENaC promoter. We conclude that DNMT3b- and MBD4-dependent methylation of the αENaC promoter limits basal αENaC transcription, in part by limiting Sp1 binding and trans-activation. Aldosterone stimulates the dispersal of DNMT3b and recruitment of Tet2 to demethylate the αENaC promoter to induce αENaC transcription. These results disclose a novel epigenetic mechanism for the control of basal and aldosterone-induced αENaC transcription that adds to previously described epigenetic controls exerted by histone modifications.
MeSH term(s)	Aldosterone/physiology ; Animals ; Azacitidine/analogs & derivatives ; Cell Line ; Cells, Cultured ; Cytosine/metabolism ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; DNA Methylation/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Decitabine ; Dioxygenases ; Endodeoxyribonucleases/genetics ; Endodeoxyribonucleases/metabolism ; Epithelial Sodium Channels/metabolism ; Kidney Tubules, Collecting/metabolism ; Mice ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Sp1 Transcription Factor/genetics ; Sp1 Transcription Factor/metabolism ; Transcription, Genetic ; DNA Methyltransferase 3B
Chemical Substances	DNA-Binding Proteins ; Epithelial Sodium Channels ; Proto-Oncogene Proteins ; Sp1 Transcription Factor ; Aldosterone (4964P6T9RB) ; Decitabine (776B62CQ27) ; Cytosine (8J337D1HZY) ; Dioxygenases (EC 1.13.11.-) ; Tet2 protein, mouse (EC 1.13.11.-) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; Endodeoxyribonucleases (EC 3.1.-) ; Mbd4 protein, mouse (EC 3.2.2.-) ; Azacitidine (M801H13NRU)
Language	English
Publishing date	2013-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00407.2013
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Article ; Online: A multinational report to characterise SARS-CoV-2 infection in people with cystic fibrosis.

Cosgriff, Rebecca / Ahern, Susannah / Bell, Scott C / Brownlee, Keith / Burgel, Pierre-Régis / Byrnes, Cass / Corvol, Harriet / Cheng, Stephanie Y / Elbert, Alexander / Faro, Albert / Goss, Christopher H / Gulmans, Vincent / Marshall, Bruce C / McKone, Edward / Middleton, Peter G / Ruseckaite, Rasa / Stephenson, Anne L / Carr, Siobhán B

Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society

2020 Volume 19, Issue 3, Page(s) 355–358

Abstract: Information is lacking on the clinical impact of the novel coronavirus, SARS-CoV-2, on people with cystic fibrosis (CF). Our aim was to characterise SARS-CoV-2 infection in people with cystic fibrosis.: Methods: Anonymised data submitted by each ... ...

Abstract	Information is lacking on the clinical impact of the novel coronavirus, SARS-CoV-2, on people with cystic fibrosis (CF). Our aim was to characterise SARS-CoV-2 infection in people with cystic fibrosis. Methods: Anonymised data submitted by each participating country to their National CF Registry was reported using a standardised template, then collated and summarised. Results: 40 cases have been reported across 8 countries. Of the 40 cases, 31 (78%) were symptomatic for SARS-CoV-2 at presentation, with 24 (60%) having a fever. 70% have recovered, 30% remain unresolved at time of reporting, and no deaths have been submitted. Conclusions: This early report shows good recovery from SARS-CoV-2 in this heterogeneous CF cohort. The disease course does not seem to differ from the general population, but the current numbers are too small to draw firm conclusions and people with CF should continue to strictly follow public health advice to protect themselves from infection.
MeSH term(s)	Adolescent ; Adult ; Australia ; Betacoronavirus ; COVID-19 ; Canada ; Coronavirus Infections/complications ; Coronavirus Infections/diagnosis ; Coronavirus Infections/therapy ; Cystic Fibrosis/complications ; Cystic Fibrosis/therapy ; Cystic Fibrosis/virology ; Europe ; Female ; Humans ; Male ; Middle Aged ; New Zealand ; Pandemics ; Pneumonia, Viral/complications ; Pneumonia, Viral/diagnosis ; Pneumonia, Viral/therapy ; SARS-CoV-2 ; Symptom Assessment ; United States ; Young Adult
Keywords	covid19
Language	English
Publishing date	2020-04-25
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2084724-5
ISSN	1873-5010 ; 1569-1993
ISSN (online)	1873-5010
ISSN	1569-1993
DOI	10.1016/j.jcf.2020.04.012
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