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A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
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Dioxin-induced thrombocyte aggregation in zebrafish.

Seongcheol Kim1, Hemalatha Sundaramoorthi1, Pudur Jagadeeswaran1

  • 1Department of Biological Sciences, University of North Texas, 1510 Chestnut, Denton TX 76203, USA.

Blood Cells, Molecules & Diseases
|August 18, 2014
PubMed
Summary
This summary is machine-generated.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) activates fish thrombocytes via the aryl hydrocarbon receptor (AHR) pathway, leading to thromboxane A2 generation. ADP also activates AHR, revealing a novel signaling mechanism.

Area of Science:

  • Environmental Toxicology
  • Cellular Biology
  • Biochemistry

Background:

  • 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a toxic environmental pollutant.
  • Dioxins, including TCDD, are known to cause abnormalities and activate platelets.
  • TCDD's mechanism for activating fish thrombocytes remains largely unknown.

Purpose of the Study:

  • To investigate the effects of TCDD on fish thrombocyte function.
  • To elucidate the molecular pathways involved in TCDD-mediated thrombocyte activation.
  • To identify potential novel activators of thrombocyte signaling.

Main Methods:

  • Zebrafish blood was used in functional assays with TCDD.
  • Thrombocyte aggregation and filopodia formation were measured.
Keywords:
ADPSignalingTCDDThrombocyteZebrafish

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  • Inhibitors targeting Gq, cyclooxygenase-1, aryl hydrocarbon receptor (AHR), c-src, Akt, and ERK1/2 were employed.

    • Main Results:

    • TCDD activated zebrafish thrombocytes, inducing aggregation and filopodia.
    • TCDD-induced activation involves AHR, c-src, Akt, ERK1/2 signaling, and thromboxane A2 generation.
    • Adenosine diphosphate (ADP) potentiated TCDD's effect and was found to activate AHR independently.

    Conclusions:

    • The study resolved the pathway of TCDD activation in thrombocytes, highlighting the roles of AHR and downstream signaling molecules.
    • ADP was identified as a novel activator of AHR in the absence of TCDD.
    • Findings contribute to understanding dioxin toxicity and thrombocyte activation mechanisms.