ToxSci Advance Access originally published online on September 26, 2006
Toxicological Sciences 2007 95(1):215-226; doi:10.1093/toxsci/kfl119
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Aryl Hydrocarbon Receptor Activation Impairs Extracellular Matrix Remodeling during Zebra Fish fin Regeneration
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* Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon 97331
Department of Veterinary Medicine, Oregon State University, Corvallis, Oregon 97331
Environmental Health Sciences Center, Oregon State University, Corvallis, Oregon 97331
Marine and Freshwater Biomedical Sciences Center, Oregon State University, Corvallis, Oregon 97331
1 To whom correspondence should be addressed at Department of Environmental and Molecular Toxicology, Oregon State University, 1007 ALS, Corvallis, OR 97331-7301. Fax: (541) 737-7966. E-mail: robert.tanguay{at}oregonstate.edu.
Received June 15, 2006; accepted September 18, 2006
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Abstract |
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Adult zebra fish 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 ECM regulation are misexpressed following activation of the aryl hydrocarbon receptor. To investigate whether TCDD blocks regeneration by impairing ECM remodeling, male zebra fish were i.p. injected with 50 ng/g TCDD or vehicle, and caudal fins were amputated. By 3 days postamputation (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 lepidotrichial-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.
Key Words: AHR; TCDD; regeneration; zebra fish; extracellular matrix.
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