Perfluorooctanesulphonicacid (PFOS), a persistent organic contaminant, has been widely detected in the environment, wildlife and humans, but few studies have assessed its effect on aquatic organisms. The present study evaluated the effect of PFOS on zebrafish embryos. Zebrafish embryos exhibited bent spine and developmental toxicity after exposure to various PFOS concentrations (0.01-16.0 μM) from 6 to 120 hour post-fertilization (hpf). The LC50 at 120 hpf was 4.39 μM and the EC50 at 120 hpf was 2.23 μM. PFOS induced apoptosis at 24 hpf was consistently located in the brain, eye, and tail region of embryos. PFOS elevated the basal rate of swimming after 4 days of exposure, and larvae exposed to PFOS (0.5-8.0μM) for only 1 h at 6 dpf swam faster with increasing PFOS concentration. Larvae exposed to 16.0 μM PFOS for 24 h periods from 1 to 121 hpf showed the highest incidence of malformations in the 97-121 hpf window. Continuous exposure to PFOS from 1 to 121 hpf resulted in a steady accumulation with no evidence of elimination. Our results further the understanding of the health risks of PFOS to aquatic organisms and identify additional research needed on PFOS toxicology.

Background: Mast cells modulate events in wound healing. Results: Shorter forms of perlecan are produced by mast cells via proteolytic processing and alternative splicing, which contain domain V and functional endorepellin. Conclusion:The production of these shorter forms modulates endothelial cell adhesion, proliferation, and migration. Significance: Mast cells produce specific forms of perlecan that affect endothelial cell behavior.

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Platelet factor 4 (PF4) is produced by platelets with roles in both inflammation and wound healing. PF4 is stored in platelet α-granules bound to the glycosaminoglycan (GAG) chains of serglycin. This study revealed that platelet serglycin is decorated with chondroitin/dermatan sulfate and that PF4 binds to these GAG chains. Additionally, PF4 had a higher affinity for endothelial-derived perlecan heparan sulfate chains than serglycin GAG chains. The binding of PF4 to perlecan was found to inhibit both FGF2 signaling and platelet activation. This study revealed additional insight into the ways in which PF4 interacts with components of the vasculature to modulate cellular events.

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