Evidence map›Paper›PMID 26553696›Full record

ArticleCirculation. Cardiovascular genetics2015

Green Tea Catechin Normalizes the Enhanced Ca2+ Sensitivity of Myofilaments Regulated by a Hypertrophic Cardiomyopathy-Associated Mutation in Human Cardiac Troponin I (K206I).

Chad M Warren, Chehade N Karam, Beata M Wolska, Tomoyoshi Kobayashi, Pieter P de Tombe, Grace M Arteaga, J Martijn Bos, Michael J Ackerman, R John Solaro

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PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation. Cardiovascular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 25 citations in OpenAlex.

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  12. Phenotyping cardiomyopathy in adult zebrafish.Progress in biophysics and molecular biology · 2018
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  16. Which way to grow? Force over time may be the heart'sGlobal cardiology science & practice · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Chad M WarrenFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
Chehade N KaramFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
Beata M WolskaFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
Tomoyoshi KobayashiFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
Pieter P de TombeFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
Grace M ArteagaFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
J Martijn BosFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
Michael J AckermanFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN.
R John SolaroFrom the Department of Physiology and Biophysics, Center for Cardiovascular Research (C.M.W., C.N.K., B.M.W., T.K., R.J.S.) and Division of Cardiology, Department of Medicine (B.M.W.), University of Illinois at Chicago; Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (P.P.d.T.); and Division of Pediatric Critical Care and Physiology, Department of Pediatrics (G.M.A.), Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (J.M.B., M.J.A.), Division of Pediatric Cardiology, Department of Pediatrics (J.M.B., M.J.A.), and Division of Cardiovascular Diseases, Department of Medicine (M.J.A.), Mayo Clinic, Rochester, MN. solarorj@uic.edu.
Loyola University Chicago · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 2000 to 2020
$42.4M
MODULATION OF CALCIUM CONTROL OF CARDIAC MYOFIBRILSR01HL022231 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUPTA, MADHU, SOLARO, R JOHN · 1985 to 2014
$2.9M
NHLBI NIH HHS P01 HL062426NHLBI NIH HHS P01HL 062426NHLBI NIH HHS R01 HL022231NHLBI NIH HHS R01 HL22231
6 · The paper itself

Abstract

backgroundHypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disease characterized by thickening of ventricular walls and decreased left ventricular chamber volume. The majority of HCM-associated mutations are found in genes encoding sarcomere proteins. Herein, we set out to functionally characterize a novel HCM-associated mutation (K206I-TNNI3) and elucidate the mechanism of dysfunction at the level of myofilament proteins. METHODS AND

resultsThe male index case was diagnosed with HCM after an out-of-hospital cardiac arrest, which was followed by comprehensive clinical evaluation, transthoracic echocardiography, and clinical genetic testing. To determine molecular mechanism(s) of the mutant human cardiac troponin I (K206I), we tested the Ca(2+) dependence of thin filament-activated myosin-S1-ATPase activity in a reconstituted, regulated, actomyosin system comparing wild-type human troponin complex, 50% mix of K206I/wildtype, or 100% K206I. We also exchanged native troponin detergent extracted fibers with reconstituted troponin containing either wildtype or a 65% mix of K206I/wildtype and measured force generation. The Ca(2+) sensitivity of the myofilaments containing the K206I variant was significantly increased, and when treated with 20 µmol/L (-)-epigallocatechin gallate (green tea) was restored back to wild-type levels in ATPase and force measurements. The K206I mutation impairs the ability of the troponin I to inhibit ATPase activity in the absence of calcium-bound human cardiac troponin C. The ability of calcium-bound human cardiac troponin C to neutralize the inhibition of K206I was greater than with wild-type TnI.

conclusionsCompromised interactions of K206I with actin and hcTnC may lead to impaired relaxation and HCM.

Indexed as

Mutation, MissenseAdolescentAmino Acid SubstitutionAnimalsCalciumCardiomyopathy, Hypertrophic, FamilialHumansMaleMiceMyofibrilsTroponin CTroponin ICalciumTroponin CTroponin Iactinactomyosincalciumechocardiographytroponin

Identifiers

PMID26553696
PMCPMC4681609
OpenAlexW2180458501

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.