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Article ; Online: Potential use of ivabradine for treatment of atrial fibrillation.

Koenig, Sara N / Mohler, Peter J

Journal of cardiovascular electrophysiology

2018 Volume 30, Issue 2, Page(s) 253–254

MeSH term(s)	Animals ; Atrial Fibrillation ; Benzazepines ; Cardiovascular Agents ; Cyclic Nucleotide-Gated Cation Channels ; Ivabradine ; Mice ; Mice, Transgenic
Chemical Substances	Benzazepines ; Cardiovascular Agents ; Cyclic Nucleotide-Gated Cation Channels ; Ivabradine (3H48L0LPZQ)
Language	English
Publishing date	2018-11-28
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1025989-2
ISSN	1540-8167 ; 1045-3873
ISSN (online)	1540-8167
ISSN	1045-3873
DOI	10.1111/jce.13788
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Article ; Online: The evolving role of ankyrin-B in cardiovascular disease.

Koenig, Sara N / Mohler, Peter J

Heart rhythm

2017 Volume 14, Issue 12, Page(s) 1884–1889

Abstract: Over the past decade, ankyrin-B has been identified as a prominent player in cardiac physiology. Ankyrin-B has a multitude of functions, with roles in expression, localization, and regulation of proteins critical for cardiac excitability, cytoskeletal ... ...

Abstract	Over the past decade, ankyrin-B has been identified as a prominent player in cardiac physiology. Ankyrin-B has a multitude of functions, with roles in expression, localization, and regulation of proteins critical for cardiac excitability, cytoskeletal integrity, and signaling. Furthermore, human ANK2 variants that result in ankyrin-B loss of function are associated with "ankyrin-B syndrome," a complex cardiac phenotype that may include bradycardia and heart rate variability, conduction block, atrial fibrillation, QT interval prolongation, and potentially fatal catecholaminergic polymorphic ventricular tachycardia. However, our understanding of the molecular mechanisms underlying ankyrin-B function at baseline and in disease is still not fully developed owing to the complexity of ankyrin-B gene regulation, number of ankyrin-B-associated molecules, multiple roles of ankyrin-B in the heart and other organs that modulate cardiac function, and a host of unexpected clinical phenotypes. In this review, we summarize known roles of ankyrin-B in the heart and the impact of ankyrin-B dysfunction in animal models and in human disease as well as highlight important new findings illustrating the complexity of ankyrin-B signaling.
MeSH term(s)	Animals ; Ankyrins/genetics ; Ankyrins/metabolism ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; DNA/genetics ; DNA Mutational Analysis ; Genetic Predisposition to Disease ; Humans ; Mutation
Chemical Substances	ANK2 protein, human ; Ankyrins ; DNA (9007-49-2)
Language	English
Publishing date	2017-07-29
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2017.07.032
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Article ; Online: Isolation and characterization of a SARS-CoV-2 variant with a Q677H mutation in the spike protein

Niu, Xiaoyu / Xu, Jiayu / Liu, Mingde / Tu, Huolin / Koenig, Sara N. / Saif, Linda J. / Jones, Daniel M. / Wang, Qiuhong

Arch Virol. 2023 Jan., v. 168, no. 1 p.5-5

2023

Abstract: We isolated 20 SARS-CoV-2 strains from positive clinical samples collected in Columbus, Ohio, and investigated the replication of one pair of isolates: a clade 20G strain and a variant of this strain carrying a Q677H mutation in the spike protein and six ...

Abstract	We isolated 20 SARS-CoV-2 strains from positive clinical samples collected in Columbus, Ohio, and investigated the replication of one pair of isolates: a clade 20G strain and a variant of this strain carrying a Q677H mutation in the spike protein and six other amino acid mutations. The OSU.20G variant replicated to a higher peak infectious titer than the 20G base strain in Vero-E6 cells, but the titers were similar when both strains were grown in Calu-3 cells. These results suggest that the OSU.20G variant has increased replication fitness compared to the 20G base strain. This may have contributed to its emergence in December 2020‐January 2021.
Keywords	Severe acute respiratory syndrome coronavirus 2 ; amino acids ; mutation ; Ohio
Language	English
Dates of publication	2023-01
Size	p. 5.
Publishing place	Springer Vienna
Document type	Article ; Online
ZDB-ID	7491-3
ISSN	1432-8798 ; 0304-8608
ISSN (online)	1432-8798
ISSN	0304-8608
DOI	10.1007/s00705-022-05621-5
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Article ; Online: Genetic basis of aortic valvular disease.

Koenig, Sara N / Lincoln, Joy / Garg, Vidu

Current opinion in cardiology

2017 Volume 32, Issue 3, Page(s) 239–245

Abstract: Purpose of review: Aortic valve disease is relatively common and encompasses both congenital and acquired forms. Bicuspid aortic valve (BAV) is the most common type of cardiac malformation and predisposes to the development of calcific aortic valve ... ...

Abstract	Purpose of review: Aortic valve disease is relatively common and encompasses both congenital and acquired forms. Bicuspid aortic valve (BAV) is the most common type of cardiac malformation and predisposes to the development of calcific aortic valve disease (CAVD). Since the description of the link between NOTCH1, BAV and CAVD approximately a decade ago, there have been significant advances in the genetic and molecular understanding of these diseases. Recent findings: Recent work has defined the congenital cardiac phenotypes linked to mutations in NOTCH1, and in addition, novel etiologic genes for BAV have been discovered using new genetic technologies in humans. Furthermore, several mouse models of BAV have been described defining the role of endothelial Notch1 in aortic valve morphogenesis, whereas others have implicated new genes. These murine models along with other cell-based studies have led to molecular insights in the pathogenesis of CAVD. Summary: These findings provide important insights into the molecular and genetic basis of aortic valve malformations, including BAV, specifically highlighting the etiologic role of endothelial cells. In addition, numerous investigations in to the mechanisms of CAVD demonstrate the importance of developmental origins and signaling pathways as well as communication between valve endothelial cells and the underlying interstitial cells in valve disease onset and progression.
Language	English
Publishing date	2017-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	645186-x
ISSN	1531-7080 ; 0268-4705
ISSN (online)	1531-7080
ISSN	0268-4705
DOI	10.1097/HCO.0000000000000384
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Article ; Online: Arrhythmogenic Cardiomyopathy: Molecular Insights for Improved Therapeutic Design.

Stevens, Tyler L / Wallace, Michael J / Refaey, Mona El / Roberts, Jason D / Koenig, Sara N / Mohler, Peter J

Journal of cardiovascular development and disease

2020 Volume 7, Issue 2

Abstract: Arrhythmogenic cardiomyopathy (ACM) is an inherited disorder characterized by structural and electrical cardiac abnormalities, including myocardial fibro-fatty replacement. Its pathological ventricular substrate predisposes subjects to an increased risk ... ...

Abstract	Arrhythmogenic cardiomyopathy (ACM) is an inherited disorder characterized by structural and electrical cardiac abnormalities, including myocardial fibro-fatty replacement. Its pathological ventricular substrate predisposes subjects to an increased risk of sudden cardiac death (SCD). ACM is a notorious cause of SCD in young athletes, and exercise has been documented to accelerate its progression. Although the genetic culprits are not exclusively limited to the intercalated disc, the majority of ACM-linked variants reside within desmosomal genes and are transmitted via Mendelian inheritance patterns; however, penetrance is highly variable. Its natural history features an initial "concealed phase" that results in patients being vulnerable to malignant arrhythmias prior to the onset of structural changes. Lack of effective therapies that target its pathophysiology renders management of patients challenging due to its progressive nature, and has highlighted a critical need to improve our understanding of its underlying mechanistic basis. In vitro and in vivo studies have begun to unravel the molecular consequences associated with disease causing variants, including altered Wnt/β-catenin signaling. Characterization of ACM mouse models has facilitated the evaluation of new therapeutic approaches. Improved molecular insight into the condition promises to usher in novel forms of therapy that will lead to improved care at the clinical bedside.
Language	English
Publishing date	2020-05-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2777082-5
ISSN	2308-3425 ; 2308-3425
ISSN (online)	2308-3425
ISSN	2308-3425
DOI	10.3390/jcdd7020021
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Article ; Online: Mechanisms and Alterations of Cardiac Ion Channels Leading to Disease: Role of Ankyrin-B in Cardiac Function.

Sucharski, Holly C / Dudley, Emma K / Keith, Caullin B R / El Refaey, Mona / Koenig, Sara N / Mohler, Peter J

Biomolecules

2020 Volume 10, Issue 2

Abstract: Ankyrin-B (encoded ... ...

Abstract	Ankyrin-B (encoded by
MeSH term(s)	Animals ; Ankyrins/genetics ; Ankyrins/physiology ; Arrhythmias, Cardiac/metabolism ; Cardiovascular Diseases/metabolism ; Cytoskeleton/metabolism ; Genetic Variation ; Heart Block ; Heart Rate ; Humans ; Ion Channels ; Phenotype ; Protein Domains ; Protein Isoforms ; Signal Transduction
Chemical Substances	ANK2 protein, human ; Ankyrins ; Ion Channels ; Protein Isoforms
Language	English
Publishing date	2020-01-31
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10020211
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Article ; Online: Humanized

Stevens, Tyler L / Manring, Heather R / Wallace, Michael J / Argall, Aaron / Dew, Trevor / Papaioannou, Peter / Antwi-Boasiako, Steve / Xu, Xianyao / Campbell, Stuart G / Akar, Fadi G / Borzok, Maegen A / Hund, Thomas J / Mohler, Peter J / Koenig, Sara N / El Refaey, Mona

Cells

2022 Volume 11, Issue 19

Abstract: Arrhythmogenic cardiomyopathy (ACM) is an inherited disorder characterized by fibro-fatty infiltration with an increased propensity for ventricular arrhythmias and sudden death. Genetic variants in desmosomal genes are associated with ACM. Incomplete ... ...

Abstract	Arrhythmogenic cardiomyopathy (ACM) is an inherited disorder characterized by fibro-fatty infiltration with an increased propensity for ventricular arrhythmias and sudden death. Genetic variants in desmosomal genes are associated with ACM. Incomplete penetrance is a common feature in ACM families, complicating the understanding of how external stressors contribute towards disease development. To analyze the dual role of genetics and external stressors on ACM progression, we developed one of the first mouse models of ACM that recapitulates a human variant by introducing the murine equivalent of the human R451G variant into endogenous desmoplakin (
MeSH term(s)	Animals ; Arrhythmias, Cardiac/genetics ; Arrhythmogenic Right Ventricular Dysplasia/genetics ; Arrhythmogenic Right Ventricular Dysplasia/metabolism ; Desmoplakins/genetics ; Disease Models, Animal ; Heart ; Humans ; Mice ; Phenotype
Chemical Substances	Desmoplakins
Language	English
Publishing date	2022-09-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11193049
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Article ; Online: Developmental origins for semilunar valve stenosis identified in mice harboring congenital heart disease-associated

LaHaye, Stephanie / Majumdar, Uddalak / Yasuhara, Jun / Koenig, Sara N / Matos-Nieves, Adrianna / Kumar, Rahul / Garg, Vidu

Disease models & mechanisms

2019 Volume 12, Issue 6

Abstract: Congenital heart defects affect ∼2% of live births and often involve malformations of the semilunar (aortic and pulmonic) valves. We previously reported a highly ... ...

Abstract	Congenital heart defects affect ∼2% of live births and often involve malformations of the semilunar (aortic and pulmonic) valves. We previously reported a highly penetrant
MeSH term(s)	Animals ; Animals, Newborn ; Aortic Valve/embryology ; Aortic Valve/metabolism ; Aortic Valve/pathology ; Aortic Valve Stenosis/genetics ; Embryo, Mammalian/abnormalities ; Embryo, Mammalian/metabolism ; Epithelial-Mesenchymal Transition ; GATA4 Transcription Factor/genetics ; GATA4 Transcription Factor/metabolism ; Gene Expression Regulation, Developmental ; Heart Defects, Congenital/genetics ; Heart Defects, Congenital/pathology ; Heterozygote ; Mice, Inbred C57BL ; Mutation/genetics ; Wnt Signaling Pathway
Chemical Substances	GATA4 Transcription Factor ; Gata4 protein, mouse
Language	English
Publishing date	2019-06-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.036764
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Article ; Online: Endothelial Notch1 Is Required for Proper Development of the Semilunar Valves and Cardiac Outflow Tract.

Koenig, Sara N / Bosse, Kevin / Majumdar, Uddalak / Bonachea, Elizabeth M / Radtke, Freddy / Garg, Vidu

Journal of the American Heart Association

2016 Volume 5, Issue 4

Abstract: Background: Congenital heart disease is the most common type of birth defect, affecting ≈2% of the population. Malformations involving the cardiac outflow tract and semilunar valves account for >50% of these cases predominantly because of a bicuspid ... ...

Abstract	Background: Congenital heart disease is the most common type of birth defect, affecting ≈2% of the population. Malformations involving the cardiac outflow tract and semilunar valves account for >50% of these cases predominantly because of a bicuspid aortic valve, which has an estimated prevalence of 1% in the population. We previously reported that mutations in NOTCH1 were a cause of bicuspid aortic valve in nonsyndromic autosomal-dominant human pedigrees. Subsequently, we described a highly penetrant mouse model of aortic valve disease, consisting of a bicuspid aortic valve with thickened cusps and associated stenosis and regurgitation, in Notch1-haploinsufficient adult mice backcrossed into a Nos3-null background. Methods and results: Here, we described the congenital cardiac abnormalities in Notch1(+/-);Nos3(-/-) embryos that led to ≈65% lethality by postnatal day 10. Although expected Mendelian ratios of Notch1(+/-);Nos3(-/-) embryos were found at embryonic day 18.5, histological examination revealed thickened, malformed semilunar valve leaflets accompanied by additional anomalies of the cardiac outflow tract including ventricular septal defects and overriding aorta. The aortic valve leaflets of Notch1(+/-);Nos3(-/-) embryos at embryonic day 15.5 were significantly thicker than controls, consistent with a defect in remodeling of the semilunar valve cushions. In addition, we generated mice haploinsufficient for Notch1 specifically in endothelial and endothelial-derived cells in a Nos3-null background and found that Notch1(fl/+);Tie2-Cre(+/-);Nos3(-/-) mice recapitulate the congenital cardiac phenotype of Notch1(+/-);Nos3(-/-) embryos. Conclusions: Our data demonstrate the role of endothelial Notch1 in the proper development of the semilunar valves and cardiac outflow tract.
MeSH term(s)	Animals ; Aortic Valve/abnormalities ; Aortic Valve/embryology ; Aortic Valve/metabolism ; Bicuspid Aortic Valve Disease ; DNA/genetics ; DNA Mutational Analysis ; Disease Models, Animal ; Endothelial Cells/metabolism ; Female ; Heart Valve Diseases/embryology ; Heart Valve Diseases/genetics ; Heart Valve Diseases/metabolism ; Heart Valves/embryology ; Male ; Mice ; Mice, Mutant Strains ; Mutation ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism
Chemical Substances	Notch1 protein, mouse ; Receptor, Notch1 ; DNA (9007-49-2)
Language	English
Publishing date	2016-04-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.115.003075
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Article ; Online: Aberrant Expression of a Non-muscle RBFOX2 Isoform Triggers Cardiac Conduction Defects in Myotonic Dystrophy.

Misra, Chaitali / Bangru, Sushant / Lin, Feikai / Lam, Kin / Koenig, Sara N / Lubbers, Ellen R / Hedhli, Jamila / Murphy, Nathaniel P / Parker, Darren J / Dobrucki, Lawrence W / Cooper, Thomas A / Tajkhorshid, Emad / Mohler, Peter J / Kalsotra, Auinash

Developmental cell

2020 Volume 52, Issue 6, Page(s) 748–763.e6

Abstract: Myotonic dystrophy type 1 (DM1) is a multisystemic genetic disorder caused by the CTG repeat expansion in the 3'-untranslated region of DMPK gene. Heart dysfunctions occur in ∼80% of DM1 patients and are the second leading cause of DM1-related deaths. ... ...

Abstract	Myotonic dystrophy type 1 (DM1) is a multisystemic genetic disorder caused by the CTG repeat expansion in the 3'-untranslated region of DMPK gene. Heart dysfunctions occur in ∼80% of DM1 patients and are the second leading cause of DM1-related deaths. Herein, we report that upregulation of a non-muscle splice isoform of RNA-binding protein RBFOX2 in DM1 heart tissue-due to altered splicing factor and microRNA activities-induces cardiac conduction defects in DM1 individuals. Mice engineered to express the non-muscle RBFOX2
MeSH term(s)	Action Potentials ; Adult ; Animals ; Cells, Cultured ; Female ; Heart Rate ; Humans ; Male ; Mice, Inbred C57BL ; Mice, Inbred ICR ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; Myotonic Dystrophy/genetics ; Myotonic Dystrophy/metabolism ; Myotonic Dystrophy/physiopathology ; Potassium Channels, Voltage-Gated/genetics ; Potassium Channels, Voltage-Gated/metabolism ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA Splicing ; RNA Splicing Factors/genetics ; RNA Splicing Factors/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Voltage-Gated Sodium Channels/genetics ; Voltage-Gated Sodium Channels/metabolism
Chemical Substances	MicroRNAs ; Potassium Channels, Voltage-Gated ; Protein Isoforms ; RBFOX2 protein, human ; RNA Splicing Factors ; Repressor Proteins ; Voltage-Gated Sodium Channels
Language	English
Publishing date	2020-02-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2020.01.037
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