Caffeine treatment disturbs the angiogenesis of zebrafish embryos

Chien-Hung Yeh1, Yun-Feng Liao, Chao-Yuan Chang

  • 1Graduate Institute of Life Sciences, Tamkang University, Tamsui, New Taipei City, Taiwan.

Insights

Caffeine intake during embryonic development can cause vascular defects. This study in zebrafish embryos revealed dose-dependent impacts on blood vessel formation, highlighting potential risks.

Area of Science:

  • Developmental Biology
  • Toxicology
  • Genetics

Background:

  • Caffeine is a common dietary substance with unclear teratogenic effects on embryonic development.
  • Understanding caffeine's impact on embryonic vascularization is crucial for public health.

Purpose of the Study:

  • To investigate caffeine-induced toxicity on embryonic vascular development using zebrafish.
  • To assess the effects of caffeine on vasculogenesis and angiogenesis in a model organism.

Main Methods:

  • Utilized a green fluorescent vascular endothelium transgenic zebrafish line (Tg(fli1:egfp)) for sensitive detection.
  • Administered varying doses of caffeine to zebrafish embryos.
  • Analyzed vascular development, including intersegmental vessels, dorsal longitudinal anastomotic vessels, and subintestinal vein sprouting.
  • Performed real-time polymerase chain reaction to analyze gene expression changes.

Main Results:

  • Caffeine treatment did not affect vasculogenesis but caused dose-dependent defects in angiogenesis.
  • Specific defects were observed in intersegmental vessels, dorsal longitudinal anastomotic vessels, and subintestinal vein sprouting at 250-350 ppm caffeine.
  • Gene expression analysis revealed upregulation of nrp1a and downregulation of sema3aa and sema3c in caffeine-treated embryos.

Conclusions:

  • Caffeine exposure during embryonic development in zebrafish leads to significant defects in angiogenesis.
  • The findings suggest caffeine's potential to disrupt complex vascular network formation.
  • Gene expression changes in nrp1a, sema3aa, and sema3c may underlie caffeine-induced vascular developmental abnormalities.

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