Mice lacking connexin45 conditionally in cardiac myocytes display embryonic lethality similar to that of germline knockout mice without endocardial cushion defect

Kiyomasa Nishii, Madoka Kumai, Katsuko Egashira, Takeshi Miwa, Kanako Hashizume, Yumi Miyano, Yosaburo Shibata

Research output: Contribution to journalArticlepeer-review

46 Citations (Scopus)

Abstract

The gap junction protein connexin45-deficient (Cx45-KO) mice die shortly after the hearts begin to beat. In addition to the heart defect, they also show defective vascular development which may be closely related with the cardiac phenotype. Therefore, we created mice whose floxed-Cx45 locus could be removed conditionally. We utilized cardiac α-actin-Cre transgenic mice to investigate the specific cardiac muscular function of Cx45 in vivo. The resultant conditional mutants were lethal, showing conduction block similar to that of the Cx45-KO mice. Unlike Cx45-KO, development of the endocardial cushion was not disrupted in the conditional mutants. X-gal staining was detected in the embryonic cardiac myocytes as a hallmark of Cre-loxP mediated floxed-Cx45 deletion. These results reconfirm the requirement of Cx45 for developing cardiac myocytes. These also indicate that establishing the first contractions is a crucial task for the early hearts.

Original languageEnglish
Pages (from-to)365-369
Number of pages5
JournalCell Communication and Adhesion
Volume10
Issue number4-6
DOIs
Publication statusPublished - 2003
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Cell Biology

Fingerprint Dive into the research topics of 'Mice lacking connexin45 conditionally in cardiac myocytes display embryonic lethality similar to that of germline knockout mice without endocardial cushion defect'. Together they form a unique fingerprint.

Cite this