Exogenous T₄ Affects Myoepithelium and Proliferation in Developing Rat Parotid

Objective: In the mature rat parotid gland, myoepithelial cells (MEC) invest intercalated ducts but not acini. However, during postnatal development, these cells differentiate around both intercalated ducts (ID) and acini, then translocate to only ID during weaning. Previously (Anat. Rec. 291:94-104, 2008), we found that thyroxine (T₄) accelerates the translocation of cells with small secretory granules from acini into ID, and apoptotic cells increased tremendously with high doses. Here we present additional analysis of T₄ effects on the distribution of MEC and the proliferation of parenchymal cells in the developing rat parotid gland. Methods: Beginning at age 4 days, pups were given daily subcutaneous injections of 0.1, 0.5 or 5 µg/g body weight of T₄ (Low, Medium and High dose groups, respectively), or vehicle or no injection (combined into one Normal group; n = 6 or more per group). At ages 4, 7, 10 and 15 days (12 for highest dose T₄), 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 (PA) was assessed via PCNA histochemistry and MEC were identified via actin histochemistry. Results: Many MEC still invested acini at 15 days in Normal glands, but few, if any, invested acini after 10 days in the T₄ groups. The PA of acinar cells and MEC in Normal glands progressively declined with age, and T₄ increased the rate of the MEC decline in a roughly dose-dependent manner. Conclusions: T₄ clearly accelerates the translocation of MEC from acini to ID, with an important mechanism being MEC PA declining more rapidly than acinar cell PA in the T₄ groups. A precipitous decline in the PA of all cells in the High and Medium T₄ groups after 7 days is attributed to thyroxine toxicity.