PUBLICATION

Aryl Hydrocarbon Receptor Activation Impairs Extracellular Matrix Remodeling during Zebra Fish fin Regeneration

Authors
Andreasen, E.A., Mathew, L.K., Lohr, C.V., Hasson, R., and Tanguay, R.L.
ID
ZDB-PUB-061222-16
Date
2007
Source
Toxicological sciences : an official journal of the Society of Toxicology   95(1): 215-226 (Journal)
Registered Authors
Andreasen, Eric A., Hasson, Rachelle, Mathew, Lijoy K., Tanguay, Robyn L.
Keywords
AHR, TCDD, regeneration, zebra fish, extracellular matrix
MeSH Terms
  • Time Factors
  • Wound Healing/drug effects*
  • Matrix Metalloproteinases/metabolism
  • Immunohistochemistry
  • Tissue Plasminogen Activator/metabolism
  • Animals
  • Enzyme Induction/drug effects
  • Carcinogens, Environmental/toxicity*
  • Male
  • Proteoglycans/metabolism
  • Polymerase Chain Reaction
  • RNA, Messenger/metabolism
  • Extremities/anatomy & histology
  • Extremities/physiology
  • Gene Expression Regulation/drug effects
  • Cytochrome P-450 CYP1A1/biosynthesis
  • Zebrafish Proteins/metabolism*
  • Transforming Growth Factor beta1/metabolism
  • Zebrafish/metabolism
  • Zebrafish/physiology*
  • Electrophoresis, Polyacrylamide Gel
  • Regeneration/drug effects*
  • Collagen/metabolism
  • Receptors, Aryl Hydrocarbon/agonists*
  • Receptors, Aryl Hydrocarbon/metabolism
  • Extracellular Matrix/metabolism*
(all 26)
PubMed
17003102 Full text @ Toxicol. Sci.
CTD
17003102
Abstract
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.
Genes / Markers
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Phenotype
Mutations / Transgenics
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Human Disease / Model
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Sequence Targeting Reagents
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Fish
Antibodies
Orthology
Engineered Foreign Genes
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Mapping