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ToxSci Advance Access published online on September 26, 2006
Toxicological Sciences, doi:10.1093/toxsci/kfl119
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received July 15, 2006
Accepted September 18, 2006

Reproductive and Developmental Toxicology

AHR Activation Impairs Extracellular Matrix Remodeling during Zebrafish Fin Regeneration

Eric A. Andreasen 1, Lijoy K. Mathew 1, Christiane Loehr 1, Rachelle Hasson 1, and Robert L. Tanguay 1 *

1 Department of Environmental and Molecular Toxicology, Department of Veterinary Medicine, Environmental Health Sciences Center, Marine and Freshwater Biomedical Sciences Center, Oregon State University, Corvallis, OR, 97331

* To whom correspondence should be addressed.
Robert L. Tanguay, E-mail: robert.tanguay{at}oregonstate.edu


  Abstract

Adult zebrafish completely regenerate their caudal (tail) fin following partial amputation. Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibits this regenerative process. Proper regulation of transcription, innervation, vascularization and extracellular matrix (ECM) composition is essential for complete fin regeneration. Previous microarray studies suggest that genes involved in extracellular matrix regulation are misexpressed following activation of the aryl hydrocarbon receptor (AHR). To investigate whether TCDD blocks regeneration by impairing extracellular matrix remodeling, male zebrafish were i.p. injected with 50 ng/g TCDD or vehicle and caudal fins were amputated. By 3 days post amputation (dpa), the vascular network in the regenerating fin of TCDD-exposed fish was disorganized compared to vehicle-exposed animals. Furthermore, immunohistochemical staining revealed that axonal outgrowth was impacted by TCDD as early as 3 dpa. Histological analysis demonstrated that TCDD exposure leads to an accumulation of collagen at the end of the fin ray just distal to the amputation site by 3 dpa. Mature lepidotrichia forming cells (fin ray forming cells) were not observed in the fins of TCDD-treated fish. The capacity to metabolize ECM was also altered by TCDD exposure. Quantitative real time PCR studies revealed that the aryl hydrocarbon pathway is active and that matrix remodeling genes are expressed in the regenerate following TCDD exposure.

Keywords: AHR; TCDD; Regeneration; Zebrafish; Extracellular Matrix.
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