Background: Thyroid damage is known to occur during experimental iodine-induced goiter. MicroRNAs (miRNAs) are a class of small non-coding RNAs regulating gene expression. Dysregulation of specific miRNAs can interfere with tissue homeostasis. The purpose of this study was to investigate the dynamic expression profiles of miRNAs during adequate or mild-excess iodine supplementation in the iodine-deficient thyroid.
Methods: Hyperplastic goiter was induced in rats by feeding a low-iodine (LI) diet for 12 weeks. Subsequently, involution of hyperplasia was obtained by administering an adequate/1- (Group 1) or 2-fold (Group 2) physiological dose of iodine for 4 weeks with a control group receiving adequate iodine intake. MiRNAs expression was analyzed in all the groups using miRNA microarray technique.
Results: In the LI group, during hyperplastic goiter formation, there were 20 miRNAs decreased and 8 increased compared to the control group. Among them, miR-708 was downregulated up to 93% and miR-144* was upregulated 8.7-fold.
After involution of the glands of Group 1 and 2, 7 common miRNAs still remained dysregulated similar to the hyperplastic phase, but 8 common miRNAs recovered to levels as found in the control group. Notably, Group 1 had more recovered miRNAs than Group 2.
Compared to the control group, some new dysregulated miRNAs emerged in Group 1 and 2 after involution. Of these, there were 6 identical miRNAs in group 1 and 2, but the amount of new misexpressing miRNAs in Group 2 was obviously larger than in Group 1. In Group 2, miR-878 was even 6-fold higher than in Group 1.
Conclusions: Our results indicate that misexpression of miRNAs is involved in iodine-induced goiter formation by a low-iodine regimen and that supplementation with adequate iodine could be more helpful to restore homeostasis than mild-excess iodine. However, further functional studies of some specific miRNAs are needed.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details unavailable.