Zebrafish crip2 plays a critical role in atrioventricular valve development by downregulating the expression of ECM genes in the endocardial cushion

Jun Dae Kim, Hey Jin Kim, Soonil Koun, Hyung Jin Ham, Myoung Jin Kim, Myungchull Rhee, Tae Lin Huh

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

The initial step of atrioventricular (AV) valve development involves the deposition of extracellular matrix (ECM) components of the endocardial cushion and the endocardial-mesenchymal transition. While the appropriately regulated expression of the major ECM components, Versican and Hyaluronan, that form the endocardial cushion is important for heart valve development, the underlying mechanism that regulates ECM gene expression remains unclear. We found that zebrafish crip2 expression is restricted to a subset of cells in the AV canal (AVC) endocardium at 55 hours post-fertilization (hpf). Knockdown of crip2 induced a heart-looping defect in zebrafish embryos, although the development of cardiac chambers appeared to be normal. In the AVC of Crip2-deficient embryos, the expression of both versican a and hyaluronan synthase 2 (has2) was highly upregulated, but the expression of bone morphogenetic protein 4 (bmp4) and T-box 2b (tbx2b) in the myocardium and of notch1b in the endocardium in the AVC did not change. Taken together, these results indicate that crip2 plays an important role in AV valve development by downregulating the expression of ECM components in the endocardial cushion.

Original languageEnglish (US)
Pages (from-to)406-411
Number of pages6
JournalMolecules and Cells
Volume37
Issue number5
DOIs
StatePublished - May 2014

Keywords

  • Cardiac valve
  • Crip2
  • Has2
  • Versican
  • Zebrafish

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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