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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Molecular characterization of thyroid hormone-inhibited atrial L-type calcium channel expression: implication for

Wei-Jan Chen1, Yung-Hsin Yeh, Kwang-Huei Lin

  • 1First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Fu-Shin Road no 5, Kwei-Shan, Tao-Yuan, Taiwan. wjchen@adm.cgmh.org.tw

Basic Research in Cardiology
|January 15, 2011
PubMed

Insights

Thyroid hormone in hyperthyroidism reduces atrial L-type calcium channel expression via a mechanism involving thyroid hormone receptor and CREB interaction. This contributes to atrial fibrillation.

Area of Science:

  • Cardiology
  • Endocrinology
  • Molecular Biology

Background:

  • Atrial fibrillation (AF) is a common complication of hyperthyroidism.
  • Thyroid hormone is known to decrease L-type calcium channel (LCC) expression, shortening action potential duration (APD) and creating a substrate for AF.

Purpose of the Study:

  • To investigate the molecular mechanism by which thyroid hormone regulates LCC expression in the atria.

Main Methods:

  • Utilized a hyperthyroid rat model and cultured murine atrial myocytes (HL-1).
  • Administered triiodothyronine (T3) and assessed LCC expression, LCC current, and APD.
  • Investigated the role of cyclic AMP response element-binding protein (CREB) and thyroid hormone receptor (TR) using transfection, chromatin immunoprecipitation, and co-immunoprecipitation assays.

Main Results:

  • T3 administration down-regulated atrial LCC expression and LCC current, abbreviating APD in HL-1 cells.
  • T3 inhibited CREB activation (phosphorylation and nuclear translocation) and reduced LCC promoter activity.
  • CRE was essential for T3-mediated LCC gene expression, and TR binding to CREB was increased by T3, inhibiting CREB activity and LCC expression.

Conclusions:

  • Thyroid hormone-induced TR binding to CREB mediates the inhibition of CREB activity and LCC expression.
  • This mechanism provides a mechanistic insight into hyperthyroidism-induced AF.

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