MicroRNAs in cardiac arrhythmia: DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

MicroRNAs in cardiac arrhythmia : DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome. / Hedley, Paula L; Carlsen, Anting L; Christiansen, Kasper M; Kanters, Jørgen K.; Behr, Elijah R; Corfield, Valerie A; Christiansen, Michael.

I: Scandinavian Journal of Clinical & Laboratory Investigation, Bind 74, Nr. 6, 08.05.2014, s. 485-491.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Hedley, PL, Carlsen, AL, Christiansen, KM, Kanters, JK, Behr, ER, Corfield, VA & Christiansen, M 2014, 'MicroRNAs in cardiac arrhythmia: DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome', Scandinavian Journal of Clinical & Laboratory Investigation, bind 74, nr. 6, s. 485-491. https://doi.org/10.3109/00365513.2014.905696

APA

Hedley, P. L., Carlsen, A. L., Christiansen, K. M., Kanters, J. K., Behr, E. R., Corfield, V. A., & Christiansen, M. (2014). MicroRNAs in cardiac arrhythmia: DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome. Scandinavian Journal of Clinical & Laboratory Investigation, 74(6), 485-491. https://doi.org/10.3109/00365513.2014.905696

Vancouver

Hedley PL, Carlsen AL, Christiansen KM, Kanters JK, Behr ER, Corfield VA o.a. MicroRNAs in cardiac arrhythmia: DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome. Scandinavian Journal of Clinical & Laboratory Investigation. 2014 maj 8;74(6):485-491. https://doi.org/10.3109/00365513.2014.905696

Author

Hedley, Paula L ; Carlsen, Anting L ; Christiansen, Kasper M ; Kanters, Jørgen K. ; Behr, Elijah R ; Corfield, Valerie A ; Christiansen, Michael. / MicroRNAs in cardiac arrhythmia : DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome. I: Scandinavian Journal of Clinical & Laboratory Investigation. 2014 ; Bind 74, Nr. 6. s. 485-491.

Bibtex

@article{8fd1442eb69f4fffbcd4dc835f97ebfc,
title = "MicroRNAs in cardiac arrhythmia: DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome",
abstract = "Long QT syndrome (LQTS) is a genetic cardiac condition associated with prolonged ventricular repolarization, primarily a result of perturbations in cardiac ion channels, which predisposes individuals to life-threatening arrhythmias. Using DNA screening and sequencing methods, over 700 different LQTS-causing mutations have been identified in 13 genes worldwide. Despite this, the genetic cause of 30-50% of LQTS is presently unknown. MicroRNAs (miRNAs) are small (∼ 22 nucleotides) noncoding RNAs which post-transcriptionally regulate gene expression by binding complementary sequences within messenger RNAs (mRNAs). The human genome encodes over 1800 miRNAs, which target about 60% of human genes. Consequently, miRNAs are likely to regulate many complex processes in the body, indeed aberrant expression of various miRNA species has been implicated in numerous disease states, including cardiovascular diseases. MiR-1 and MiR-133A are the most abundant miRNAs in the heart and have both been reported to regulate cardiac ion channels. We hypothesized that, as a consequence of their role in regulating cardiac ion channels, genetic variation in the genes which encode MiR-1 and MiR-133A might explain some cases of LQTS. Four miRNA genes (miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2), which encode MiR-1 and MiR-133A, were sequenced in 125 LQTS probands. No genetic variants were identified in miR-1-1 or miR-133a-1; but in miR-1-2 we identified a single substitution (n.100A> G) and in miR-133a-2 we identified two substitutions (n.-19G> A and n.98C> T). None of the variants affect the mature miRNA products. Our findings indicate that sequence variants of miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2 are not a cause of LQTS in this cohort.",
author = "Hedley, {Paula L} and Carlsen, {Anting L} and Christiansen, {Kasper M} and Kanters, {J{\o}rgen K.} and Behr, {Elijah R} and Corfield, {Valerie A} and Michael Christiansen",
year = "2014",
month = may,
day = "8",
doi = "10.3109/00365513.2014.905696",
language = "English",
volume = "74",
pages = "485--491",
journal = "Scandinavian Journal of Clinical & Laboratory Investigation",
issn = "0036-5513",
publisher = "Taylor & Francis",
number = "6",

}

RIS

TY - JOUR

T1 - MicroRNAs in cardiac arrhythmia

T2 - DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome

AU - Hedley, Paula L

AU - Carlsen, Anting L

AU - Christiansen, Kasper M

AU - Kanters, Jørgen K.

AU - Behr, Elijah R

AU - Corfield, Valerie A

AU - Christiansen, Michael

PY - 2014/5/8

Y1 - 2014/5/8

N2 - Long QT syndrome (LQTS) is a genetic cardiac condition associated with prolonged ventricular repolarization, primarily a result of perturbations in cardiac ion channels, which predisposes individuals to life-threatening arrhythmias. Using DNA screening and sequencing methods, over 700 different LQTS-causing mutations have been identified in 13 genes worldwide. Despite this, the genetic cause of 30-50% of LQTS is presently unknown. MicroRNAs (miRNAs) are small (∼ 22 nucleotides) noncoding RNAs which post-transcriptionally regulate gene expression by binding complementary sequences within messenger RNAs (mRNAs). The human genome encodes over 1800 miRNAs, which target about 60% of human genes. Consequently, miRNAs are likely to regulate many complex processes in the body, indeed aberrant expression of various miRNA species has been implicated in numerous disease states, including cardiovascular diseases. MiR-1 and MiR-133A are the most abundant miRNAs in the heart and have both been reported to regulate cardiac ion channels. We hypothesized that, as a consequence of their role in regulating cardiac ion channels, genetic variation in the genes which encode MiR-1 and MiR-133A might explain some cases of LQTS. Four miRNA genes (miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2), which encode MiR-1 and MiR-133A, were sequenced in 125 LQTS probands. No genetic variants were identified in miR-1-1 or miR-133a-1; but in miR-1-2 we identified a single substitution (n.100A> G) and in miR-133a-2 we identified two substitutions (n.-19G> A and n.98C> T). None of the variants affect the mature miRNA products. Our findings indicate that sequence variants of miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2 are not a cause of LQTS in this cohort.

AB - Long QT syndrome (LQTS) is a genetic cardiac condition associated with prolonged ventricular repolarization, primarily a result of perturbations in cardiac ion channels, which predisposes individuals to life-threatening arrhythmias. Using DNA screening and sequencing methods, over 700 different LQTS-causing mutations have been identified in 13 genes worldwide. Despite this, the genetic cause of 30-50% of LQTS is presently unknown. MicroRNAs (miRNAs) are small (∼ 22 nucleotides) noncoding RNAs which post-transcriptionally regulate gene expression by binding complementary sequences within messenger RNAs (mRNAs). The human genome encodes over 1800 miRNAs, which target about 60% of human genes. Consequently, miRNAs are likely to regulate many complex processes in the body, indeed aberrant expression of various miRNA species has been implicated in numerous disease states, including cardiovascular diseases. MiR-1 and MiR-133A are the most abundant miRNAs in the heart and have both been reported to regulate cardiac ion channels. We hypothesized that, as a consequence of their role in regulating cardiac ion channels, genetic variation in the genes which encode MiR-1 and MiR-133A might explain some cases of LQTS. Four miRNA genes (miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2), which encode MiR-1 and MiR-133A, were sequenced in 125 LQTS probands. No genetic variants were identified in miR-1-1 or miR-133a-1; but in miR-1-2 we identified a single substitution (n.100A> G) and in miR-133a-2 we identified two substitutions (n.-19G> A and n.98C> T). None of the variants affect the mature miRNA products. Our findings indicate that sequence variants of miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2 are not a cause of LQTS in this cohort.

U2 - 10.3109/00365513.2014.905696

DO - 10.3109/00365513.2014.905696

M3 - Journal article

C2 - 24809446

VL - 74

SP - 485

EP - 491

JO - Scandinavian Journal of Clinical & Laboratory Investigation

JF - Scandinavian Journal of Clinical & Laboratory Investigation

SN - 0036-5513

IS - 6

ER -

ID: 117087586