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Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac

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Trichloroethylene (TCE) exposure causes congenital heart disease (CHD) by down-regulating the gremlin1 gene, leading to mitochondrial dysfunction and abnormal heart development in zebrafish.

Keywords:
Cardiac defectsGremlin1Mitochondrial hyperfunctionSingle-cell RNA sequencingTrichloroethylene

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Area of Science:

  • Developmental Biology
  • Toxicology
  • Genetics

Background:

  • Trichloroethylene (TCE) is a widespread environmental pollutant.
  • TCE exposure is linked to congenital heart disease (CHD), but underlying mechanisms are unclear.

Purpose of the Study:

  • Investigate TCE's cardiac toxicity and mechanisms in zebrafish.
  • Identify genetic factors contributing to TCE-induced CHD.

Main Methods:

  • Zebrafish embryos exposed to TCE.
  • Bulk and single-cell RNA sequencing (scRNA-seq) used.
  • CRISPR/dCas9 system employed for genetic analysis.

Main Results:

  • TCE exposure caused cardiac defects (elongated SV-BA distance, thin myocardium).
  • TCE significantly downregulated the gremlin1 gene (grem1a).
  • grem1a knockdown mimicked TCE's cardiac defects; enhanced mitochondrial respiration and disrupted myofibril development observed.

Conclusions:

  • TCE-induced gremlin1 repression leads to mitochondrial hyperfunction, impairing cardiomyocyte development and causing CHD.
  • This study reveals a novel mechanism for environmental stressor-induced cardiac defects.
  • Gremlin1 repression presents a potential therapeutic target for TCE-induced CHD.