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Updated: Jun 17, 2026
06:38
Mechanical Vessel Injury in Zebrafish Embryos
Published on: February 17, 2015
Evolution of primary hemostasis in early vertebrates
Seongcheol Kim1, Maira Carrillo, Vrinda Kulkarni
1Department of Biological Sciences, University of North Texas, Denton, Texas, USA.
Plos One
|December 29, 2009
Summary
Fish gills release active trypsins that activate thrombocytes, preventing bleeding. This study reveals trypsin
Area of Science:
- Comparative physiology
- Evolutionary biology
- Biochemistry
Background:
- Hemostasis is a vital defense mechanism against bleeding.
- Major mammalian hemostatic factors are conserved in early vertebrates.
- Fish gills, with high blood pressure and environmental exposure, are vulnerable to fatal bleeding.
Purpose of the Study:
- To investigate the role of trypsin in fish gill hemostasis.
- To identify trypsin-like proteases released by fish gills.
- To explore the mechanism of trypsin-mediated bleeding protection in fish.
Main Methods:
- Identification and characterization of trypsins released from fish gills.
- Assay of serine protease activity of fish trypsins.
- Analysis of zebrafish genome to identify protease-activated receptors (PARs).
- Functional assay of PAR2 activation by trypsin and its effect on gill bleeding.
Main Results:
- Three distinct trypsins with high serine protease activity were released from fish gills.
- These trypsins were found to activate thrombocytes and prevent gill bleeding.
- Twenty-seven protease-activated receptors (PARs) were identified in zebrafish, classified into PAR1 and PAR2 families.
- A specific PAR2 member, PAR2-21A, was activated by trypsin, and its peptide motif inhibited gill bleeding.
Conclusions:
- Fish gills are evolutionarily adapted to produce trypsin to activate PAR2 on thrombocytes, ensuring gill hemostasis.
- Trypsin-mediated activation of PAR2 likely plays a crucial role in primary hemostasis in early vertebrates.
- Trypsin may also contribute to hemostasis in other injuries in fish.
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