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Research Article

Exogenous thyroid hormone affects myoepithelium and proliferation in the developing rat parotid gland

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Pages 267-274 | Accepted 09 Apr 2009, Published online: 08 Jan 2010
 

Abstract

In the mature rat parotid gland, myoepithelial cells (MEC) invest intercalated ducts, but not acini. During postnatal development, however, these cells differentiate around both intercalated ducts and acini, then translocate to only intercalated ducts during weaning. Previously, we found that thyroxine (T4) accelerates translocation of cells with small secretory granules from acini into intercalated ducts and the number of apoptotic cells increased tremendously with high doses. We present here additional analysis of the effects of T4 on developing rat parotid gland, namely, the distribution of MEC and the proliferation of parenchymal cells. Beginning at age four days, pups were given daily subcutaneous injections of low, medium, and high doses of T4 or vehicle or no injection. At ages 4, 7, 10, and 15 days, glands were excised and processed for light microscopy. Sections were double-immunostained with antibodies against proliferating cell nuclear antigen (PCNA) and actin, and counterstained with hematoxylin. Proliferative activity was assessed via PCNA histochemistry and MEC were identified using actin histochemistry. MEC in the T4 groups invested mostly acini at 15 days in vehicle/normal glands and mostly intercalated ducts after 10 days in the T4 groups. The proliferative activity of acinar cells and MEC in vehicle/normal glands declined progressively with age and T4 increased the rate of this decline in the MEC in a dose-dependent manner. We conclude that T4 accelerates the translocation of MEC from acini to intercalated ducts and that an important mechanism is the more rapid decline in the proliferative activity of MEC than in acinar cells in the T4 groups. Some of the decline in the proliferative activity of all cells in the high and medium dose T4 groups after seven days may have been due to dose-related thyroxine toxicity.

Acknowledgments

This research was supported in part by The Nippon Dental University, Tokyo, Japan (RI), Grant DE 14995 from The National Institute of Dental and Craniofacial Research, The National Institutes of Health, Bethesda, MD (RSR), and the Research Service of the Department of Veterans Affairs Medical Center, Washington, DC. We thank Ms Sumie Satoh for her technical assistance.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

ERRATUM

[ePub ahead of print] 25 May 2009, DOI: 10.1080/10520290902984258 The Early Online version of this article published ahead of print on 25 May 2009 contained errors in the footnotes to Table 1–3. The footnotes were out of sequence with the citations in the body of the table. The corrected version is shown in this issue.

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