ZFIN ID: ZDB-PUB-100427-1
Implication of type 3 deiodinase induction in zebrafish fin regeneration
Bouzaffour, M., Rampon, C., Ramaugé, M., Courtin, F., and Vriz, S.
Date: 2010
Source: General and comparative endocrinology   168(1): 88-94 (Journal)
Registered Authors: Vriz, Sophie
Keywords: Fin regeneration, Deiodinase, Thyroid hormone, Zebrafish
MeSH Terms:
  • Animals
  • Antithyroid Agents/pharmacology
  • Iodide Peroxidase/genetics
  • Iodide Peroxidase/metabolism*
  • Methimazole/pharmacology
  • Regeneration/drug effects*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Thyroid Hormones/metabolism
  • Zebrafish/metabolism*
  • Zebrafish/physiology*
PubMed: 20403357 Full text @ Gen. Comp. Endocrinol.
Thyroid hormones are critical determinants of cellular differentiation. We used the zebrafish model to evaluate the involvement of thyroid hormones in regeneration processes after caudal fin amputation. We examined early events following fin amputation, i.e., blastema formation and nerve repair by growth cone formation. Here, we show that the abolition of thyroid gland activity by methimazole treatment had no effect on blastema formation, but slowed growth cone formation of the lateral line. Conversely, the addition of exogenous thyroid hormones enhanced growth cone formation without affecting blastema formation. However, amputation triggered a strong induction in the blastema of type 3 deiodinase mRNA and enzymatic activity, which degrades thyroid hormone (TH). We therefore blocked deiodinase activity with iopanoic acid (IOP) and saw a reduction in blastema formation, suggesting that local degradation of TH is permissive for cell proliferation in the blastema. The effect of IOP on the blastema required endogenous or exogenous TH. Our findings support a model in which local degradation of TH by type 3 deiodinase is permissive for epimorphic regeneration.