Altered function in atrium of transgenic mice overexpressing triadin 1

Uwe Kirchhefer, Hideo A. Baba, Yvonne M. Kobayashi, Larry Jones, Wilhelm Schmitz, Joachim Neumann

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Triadin 1 is a protein in the cardiac junctional sarcoplasmic reticulum (SR) that interacts with the ryanodine receptor, junctin, and calsequestrin, proteins that are important for Ca2+ release. To better understand the role of triadin 1 in SR-Ca2+ release, we studied the time-dependent expression of SR proteins and contractility in atria of 3-, 6-, and 18-wk-old transgenic mice overexpressing canine cardiac triadin 1 under control of the α-myosin heavy chain (MHC) promoter. Three-week-old transgenic atria exhibited mild hypertrophy. Finally, atrial weight was increased by 110% in 18-wk-old transgenic mice. Triadin 1 overexpression was accompanied by time-dependent changes in the protein expression of the ryanodine receptor, junctin, and cardiac/slow-twitch muscle SR Ca2+-ATPase isoform. Force of contraction was already decreased in 3-wk-old transgenic atria. The application of caffeine led to a positive inotropic effect in transgenic atria of 3-wk-old mice. Rest pauses resulted in an increased potentiation of force of contraction after restimulation in 3- and 6-wk-old mice and a reduced potentiation of force of contraction in 18-wk-old transgenic mice. Hence, triadin 1 overexpression triggered time-dependent alterations in SR protein expression, Ca2+ homeostasis, and contractility, indicating for the first time an inhibitory function of triadin 1 on SR-Ca2+ release in vivo.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume283
Issue number4 52-4
StatePublished - Oct 2002

Fingerprint

Sarcoplasmic Reticulum
Transgenic Mice
Ryanodine Receptor Calcium Release Channel
Proteins
Calsequestrin
Calcium-Transporting ATPases
Myosin Heavy Chains
Caffeine
Hypertrophy
triadin
Canidae
Protein Isoforms
Homeostasis
Weights and Measures
Muscles

Keywords

  • Force of contraction
  • Protein expression
  • Sarcoplasmic reticulum-calcium release

ASJC Scopus subject areas

  • Physiology

Cite this

Kirchhefer, U., Baba, H. A., Kobayashi, Y. M., Jones, L., Schmitz, W., & Neumann, J. (2002). Altered function in atrium of transgenic mice overexpressing triadin 1. American Journal of Physiology - Heart and Circulatory Physiology, 283(4 52-4).

Altered function in atrium of transgenic mice overexpressing triadin 1. / Kirchhefer, Uwe; Baba, Hideo A.; Kobayashi, Yvonne M.; Jones, Larry; Schmitz, Wilhelm; Neumann, Joachim.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 283, No. 4 52-4, 10.2002.

Research output: Contribution to journalArticle

Kirchhefer, U, Baba, HA, Kobayashi, YM, Jones, L, Schmitz, W & Neumann, J 2002, 'Altered function in atrium of transgenic mice overexpressing triadin 1', American Journal of Physiology - Heart and Circulatory Physiology, vol. 283, no. 4 52-4.
Kirchhefer, Uwe ; Baba, Hideo A. ; Kobayashi, Yvonne M. ; Jones, Larry ; Schmitz, Wilhelm ; Neumann, Joachim. / Altered function in atrium of transgenic mice overexpressing triadin 1. In: American Journal of Physiology - Heart and Circulatory Physiology. 2002 ; Vol. 283, No. 4 52-4.
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