Diabetes decreases mRNA levels of calcium-release channels in human atrial appendage

Sahika Guner, Ebru Arioglu, Aydin Tay, Atalay Tasdelen, Sait Aslamaci, Keshore R Bidasee, Umit Deniz Dincer

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Patients with chronic diabetes mellitus usually develop reductions in rate and force of cardiac contractions. Since calcium-release channels (ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs)) play integral roles in effecting these processes, we rationalize that alterations in their expression may underlie these defects. To test this hypothesis, right atrial appendages were obtained from diabetic (65.0 ± 4.5 years) and nondiabetic (56.2 ± 2.6 years) patients undergoing coronary arterial by-pass grafting and reverse transcription-polymerase chain reactions were used to compare steady state levels of mRNA encoding the three major isoforms of RyRs and IP3Rs. In this study we did not detect either RyR1 or RyR3 in human atrial appendage. When compared with nondiabetic patients, mRNA encoding RyR2 from diabetic patients decreased by 74.2 ± 6.2% (p < 0.01). Diabetes also significantly decreased steady-state levels of mRNA encoding the IP3Rs in human atrial appendage. IP3R1 decreased by 24.2 ± 4.6%, IP3R2 decreased by 63.0 ± 4.6% and IP3R3 decreased by 55.5 ± 6.5%. Since a reduction in steady-state mRNA is usually indicative of a decrease in protein levels, these data suggest that the decrease in chronotropy and inotropy seen in chronic diabetic patients may be due in part to a decrease in expression of calcium-release channels.

Original languageEnglish (US)
Pages (from-to)143-150
Number of pages8
JournalMolecular and cellular biochemistry
Volume263
Issue number1
DOIs
StatePublished - Aug 1 2004

Fingerprint

Atrial Appendage
Ryanodine Receptor Calcium Release Channel
Calcium Channels
Medical problems
Calcium
Messenger RNA
Inositol 1,4,5-Trisphosphate Receptors
Polymerase chain reaction
Inositol
Transcription
Reverse Transcription
Diabetes Mellitus
Protein Isoforms
Polymerase Chain Reaction
Defects
Proteins

Keywords

  • 1,4,5-trisphosphate receptors
  • Calcium-release channels
  • Diabetes
  • Expression
  • Human atrial appendage
  • Inositol
  • Reverse transcription-polymerase chain reaction
  • Ryanodine receptors

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Diabetes decreases mRNA levels of calcium-release channels in human atrial appendage. / Guner, Sahika; Arioglu, Ebru; Tay, Aydin; Tasdelen, Atalay; Aslamaci, Sait; Bidasee, Keshore R; Dincer, Umit Deniz.

In: Molecular and cellular biochemistry, Vol. 263, No. 1, 01.08.2004, p. 143-150.

Research output: Contribution to journalArticle

Guner, Sahika ; Arioglu, Ebru ; Tay, Aydin ; Tasdelen, Atalay ; Aslamaci, Sait ; Bidasee, Keshore R ; Dincer, Umit Deniz. / Diabetes decreases mRNA levels of calcium-release channels in human atrial appendage. In: Molecular and cellular biochemistry. 2004 ; Vol. 263, No. 1. pp. 143-150.
@article{c645939a1210430489290a1716fe16b6,
title = "Diabetes decreases mRNA levels of calcium-release channels in human atrial appendage",
abstract = "Patients with chronic diabetes mellitus usually develop reductions in rate and force of cardiac contractions. Since calcium-release channels (ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs)) play integral roles in effecting these processes, we rationalize that alterations in their expression may underlie these defects. To test this hypothesis, right atrial appendages were obtained from diabetic (65.0 ± 4.5 years) and nondiabetic (56.2 ± 2.6 years) patients undergoing coronary arterial by-pass grafting and reverse transcription-polymerase chain reactions were used to compare steady state levels of mRNA encoding the three major isoforms of RyRs and IP3Rs. In this study we did not detect either RyR1 or RyR3 in human atrial appendage. When compared with nondiabetic patients, mRNA encoding RyR2 from diabetic patients decreased by 74.2 ± 6.2{\%} (p < 0.01). Diabetes also significantly decreased steady-state levels of mRNA encoding the IP3Rs in human atrial appendage. IP3R1 decreased by 24.2 ± 4.6{\%}, IP3R2 decreased by 63.0 ± 4.6{\%} and IP3R3 decreased by 55.5 ± 6.5{\%}. Since a reduction in steady-state mRNA is usually indicative of a decrease in protein levels, these data suggest that the decrease in chronotropy and inotropy seen in chronic diabetic patients may be due in part to a decrease in expression of calcium-release channels.",
keywords = "1,4,5-trisphosphate receptors, Calcium-release channels, Diabetes, Expression, Human atrial appendage, Inositol, Reverse transcription-polymerase chain reaction, Ryanodine receptors",
author = "Sahika Guner and Ebru Arioglu and Aydin Tay and Atalay Tasdelen and Sait Aslamaci and Bidasee, {Keshore R} and Dincer, {Umit Deniz}",
year = "2004",
month = "8",
day = "1",
doi = "10.1023/B:MCBI.0000041856.92497.0c",
language = "English (US)",
volume = "263",
pages = "143--150",
journal = "Molecular and Cellular Biochemistry",
issn = "0300-8177",
publisher = "Springer Netherlands",
number = "1",

}

TY - JOUR

T1 - Diabetes decreases mRNA levels of calcium-release channels in human atrial appendage

AU - Guner, Sahika

AU - Arioglu, Ebru

AU - Tay, Aydin

AU - Tasdelen, Atalay

AU - Aslamaci, Sait

AU - Bidasee, Keshore R

AU - Dincer, Umit Deniz

PY - 2004/8/1

Y1 - 2004/8/1

N2 - Patients with chronic diabetes mellitus usually develop reductions in rate and force of cardiac contractions. Since calcium-release channels (ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs)) play integral roles in effecting these processes, we rationalize that alterations in their expression may underlie these defects. To test this hypothesis, right atrial appendages were obtained from diabetic (65.0 ± 4.5 years) and nondiabetic (56.2 ± 2.6 years) patients undergoing coronary arterial by-pass grafting and reverse transcription-polymerase chain reactions were used to compare steady state levels of mRNA encoding the three major isoforms of RyRs and IP3Rs. In this study we did not detect either RyR1 or RyR3 in human atrial appendage. When compared with nondiabetic patients, mRNA encoding RyR2 from diabetic patients decreased by 74.2 ± 6.2% (p < 0.01). Diabetes also significantly decreased steady-state levels of mRNA encoding the IP3Rs in human atrial appendage. IP3R1 decreased by 24.2 ± 4.6%, IP3R2 decreased by 63.0 ± 4.6% and IP3R3 decreased by 55.5 ± 6.5%. Since a reduction in steady-state mRNA is usually indicative of a decrease in protein levels, these data suggest that the decrease in chronotropy and inotropy seen in chronic diabetic patients may be due in part to a decrease in expression of calcium-release channels.

AB - Patients with chronic diabetes mellitus usually develop reductions in rate and force of cardiac contractions. Since calcium-release channels (ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs)) play integral roles in effecting these processes, we rationalize that alterations in their expression may underlie these defects. To test this hypothesis, right atrial appendages were obtained from diabetic (65.0 ± 4.5 years) and nondiabetic (56.2 ± 2.6 years) patients undergoing coronary arterial by-pass grafting and reverse transcription-polymerase chain reactions were used to compare steady state levels of mRNA encoding the three major isoforms of RyRs and IP3Rs. In this study we did not detect either RyR1 or RyR3 in human atrial appendage. When compared with nondiabetic patients, mRNA encoding RyR2 from diabetic patients decreased by 74.2 ± 6.2% (p < 0.01). Diabetes also significantly decreased steady-state levels of mRNA encoding the IP3Rs in human atrial appendage. IP3R1 decreased by 24.2 ± 4.6%, IP3R2 decreased by 63.0 ± 4.6% and IP3R3 decreased by 55.5 ± 6.5%. Since a reduction in steady-state mRNA is usually indicative of a decrease in protein levels, these data suggest that the decrease in chronotropy and inotropy seen in chronic diabetic patients may be due in part to a decrease in expression of calcium-release channels.

KW - 1,4,5-trisphosphate receptors

KW - Calcium-release channels

KW - Diabetes

KW - Expression

KW - Human atrial appendage

KW - Inositol

KW - Reverse transcription-polymerase chain reaction

KW - Ryanodine receptors

UR - http://www.scopus.com/inward/record.url?scp=4544244614&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4544244614&partnerID=8YFLogxK

U2 - 10.1023/B:MCBI.0000041856.92497.0c

DO - 10.1023/B:MCBI.0000041856.92497.0c

M3 - Article

VL - 263

SP - 143

EP - 150

JO - Molecular and Cellular Biochemistry

JF - Molecular and Cellular Biochemistry

SN - 0300-8177

IS - 1

ER -