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Updated: Jul 14, 2026

Heart Dissection in Larval, Juvenile and Adult Zebrafish, Danio rerio
06:43

Heart Dissection in Larval, Juvenile and Adult Zebrafish, Danio rerio

Published on: September 30, 2011

Lrrc10 is required for early heart development and function in zebrafish.

Ki-Hyun Kim1, Dagmara S Antkiewicz, Long Yan

  • 1Department of Anatomy, School of Medicine and Public Health, University of Wisconsin, 1300 University Avenue, Madison, WI 53706, USA.

Developmental Biology
|July 3, 2007
PubMed
Summary

Leucine-rich repeat containing protein 10 (LRRC10) is crucial for zebrafish heart development. Knocking down LRRC10 causes severe cardiac defects and embryonic lethality, highlighting its role in cardiac function.

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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Zebrafish Models

Background:

  • Leucine-rich repeat containing protein 10 (LRRC10) is a recently identified cardiac-specific factor in mice.
  • The precise function of LRRC10 in cardiac development and function remains largely unknown.

Purpose of the Study:

  • To investigate the developmental roles and functional significance of LRRC10 in cardiac development using zebrafish.
  • To elucidate the underlying molecular mechanisms contributing to cardiac defects observed upon Lrrc10 knockdown.

Main Methods:

  • Morpholino-mediated knockdown of Lrrc10 in zebrafish embryos.
  • Assessment of cardiac morphology and function using live imaging and echocardiography.
  • Analysis of cardiomyocyte number and expression of key cardiac genes.

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Last Updated: Jul 14, 2026

Heart Dissection in Larval, Juvenile and Adult Zebrafish, Danio rerio
06:43

Heart Dissection in Larval, Juvenile and Adult Zebrafish, Danio rerio

Published on: September 30, 2011

Large-scale Zebrafish Embryonic Heart Dissection for Transcriptional Analysis
10:00

Large-scale Zebrafish Embryonic Heart Dissection for Transcriptional Analysis

Published on: January 12, 2015

Isolation and Characterization of Single Cells from Zebrafish Embryos
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Published on: March 12, 2016

  • Measurement of NADH fluorescence in the heart.
  • Main Results:

    • Lrrc10 knockdown resulted in severe cardiac morphogenic defects, including looping failure and pericardial edema, leading to embryonic lethality.
    • Morphant zebrafish exhibited impaired cardiac function, characterized by reduced ejection fraction and cardiac output.
    • A significant reduction in cardiomyocyte number and deregulation of cardiac gene expression (increased atrial natriuretic factor, decreased cardiac myosin light chain 2) were observed.
    • Reduced NADH fluorescence in the morphant heart suggests mitochondrial dysfunction.

    Conclusions:

    • Lrrc10 is essential for normal cardiac development and function in zebrafish embryos.
    • These findings provide critical insights into the role of LRRC10 in congenital heart defects and broader heart disease research.