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Related Experiment Video

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Analysis of Cardiac Chamber Development During Mouse Embryogenesis Using Whole Mount Epifluorescence
06:27

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Published on: April 17, 2019

Krüppel-like factor 2 is required for normal mouse cardiac development.

Aditi R Chiplunkar1, Tina K Lung, Yousef Alhashem

  • 1Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia, United States of America.

Plos One
|March 5, 2013
PubMed
Summary

Krüppel-like factor 2 (KLF2) is crucial for early heart development and endothelial to mesenchymal transformation (EMT) in mice. Its absence causes severe cardiac defects, with phenotypes varying by genetic background.

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Area of Science:

  • Developmental Biology
  • Cardiovascular Research
  • Gene Regulation

Background:

  • Krüppel-like factor 2 (KLF2) is known to be expressed in endothelial cells under high shear stress.
  • Previous studies indicated KLF2's role in later stages of cardiac development, with ablation causing heart failure by embryonic day 14.5 in mixed genetic backgrounds.
  • The precise role of KLF2 in early heart development and its genetic background dependency were not fully understood.

Purpose of the Study:

  • To investigate the fundamental role of Krüppel-like factor 2 (KLF2) in early mouse cardiac development.
  • To determine the impact of KLF2 deficiency on endothelial to mesenchymal transformation (EMT) in the developing heart.
  • To explore the genetic background-specific effects of KLF2 ablation on cardiac development.

Main Methods:

  • Utilized KLF2 knockout (KLF2-/-) mouse models on FVB/N and C57BL/6 genetic backgrounds.
  • Examined embryonic hearts at various stages (E9.5, E10.5, E11.5) using histological analysis.
  • Performed echocardiography to assess cardiac function and chromatin immunoprecipitation assays to identify gene targets.

Main Results:

  • FVB/N KLF2-/- embryos exhibited earlier lethality (E11.5) and severe defects in atrioventricular (AV) cushion development, characterized by disorganized and hypocellular layers.
  • A significant defect in endothelial to mesenchymal transformation (EMT) was observed in FVB/N KLF2-/- hearts, with reduced glycosaminoglycans and impaired mesenchymal cell migration.
  • KLF2 ablation led to delayed atrial septum formation in both FVB/N and C57BL/6 backgrounds, and altered expression of key cardiac genes (Sox9, Ugdh, Gata4, Tbx5), with KLF2 directly binding to their promoters.

Conclusions:

  • Krüppel-like factor 2 (KLF2) plays a critical and earlier role in mouse cardiac development than previously recognized, particularly in AV cushion formation and EMT.
  • The cardiac phenotype resulting from KLF2 deficiency is significantly dependent on the genetic background.
  • KLF2 regulates crucial cardiovascular genes, including Gata4, Tbx5, and Ugdh, thereby influencing endothelial to mesenchymal transformation during heart development.