Heterozygous deletion of sarcolipin maintains normal cardiac function

Daisuke Shimura, Yoichiro Kusakari, Tetsuo Sasano, Yasuhiro Nakashima, Gaku Nakai, Qibin Jiao, Meihua Jin, Tomohiro Yokota, Yoshihiro Ishikawa, Atsushi Nakano, Nobuhito Goda, Susumu Minamisawa

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Sarcolipin (SLN) is a small proteolipid and a regulator of sarco(endo)plasmic reticulum Ca2+-ATPase. In heart tissue, SLN is exclusively expressed in the atrium. Previously, we inserted Cre recombinase into the endogenous SLN locus by homologous recombination and succeeded in generating SLN-Cre knockin (SlnCre/+) mice. This SlnCre/+ mouse can be used to generate an atrium-specific gene-targeting mutant, and it is based on the Cre-loxP system. In the present study, we used adult SlnCre/+ mice atria and analyzed the effects of heterozygous SLN deletion by Cre knockin before use as the gene targeting mouse. Both SLN mRNA and protein levels were decreased in SlnCre/+ mouse atria, but there were no morphological, physiological, or molecular biological abnormalities. The properties of contractility and Ca2+ handling were similar to wild-type (WT) mice, and expression levels of several stress markers and sarcoplasmic reticulum-related protein levels were not different between SlnCre/+ and WT mice. Moreover, there was no significant difference in sarco(endo)plasmic reticulum Ca2+-ATPase activity between the two groups. We showed that SlnCre/+ mice were not significantly different from WT mice in all aspects that were examined. The present study provides basic characteristics of SlnCre/+ mice and possibly information on the usefulness of SlnCre/+ mice as an atrium-specific gene-targeting model.

Original languageEnglish
Pages (from-to)H92-H103
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume310
Issue number1
DOIs
Publication statusPublished - 2016 Jan

Keywords

  • Atrium
  • Calcium homeostasis
  • Cre knockin
  • Sarcoplasmic reticulum

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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  • Cite this

    Shimura, D., Kusakari, Y., Sasano, T., Nakashima, Y., Nakai, G., Jiao, Q., Jin, M., Yokota, T., Ishikawa, Y., Nakano, A., Goda, N., & Minamisawa, S. (2016). Heterozygous deletion of sarcolipin maintains normal cardiac function. American Journal of Physiology - Heart and Circulatory Physiology, 310(1), H92-H103. https://doi.org/10.1152/ajpheart.00411.2015