Document Detail


Exogenous thyroid hormone affects myoepithelium and proliferation in the developing rat parotid gland.
MedLine Citation:
PMID:  19468923     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 (T(4)) 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 T(4) 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 T(4) 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 T(4) groups invested mostly acini at 15 days in vehicle/normal glands and mostly intercalated ducts after 10 days in the T(4) groups. The proliferative activity of acinar cells and MEC in vehicle/normal glands declined progressively with age and T(4) increased the rate of this decline in the MEC in a dose-dependent manner. We conclude that T(4) 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 T(4) groups. Some of the decline in the proliferative activity of all cells in the high and medium dose T(4) groups after seven days may have been due to dose-related thyroxine toxicity.
Authors:
R Ikeda; S Aiyama; R S Redman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Biotechnic & histochemistry : official publication of the Biological Stain Commission     Volume:  84     ISSN:  1473-7760     ISO Abbreviation:  Biotech Histochem     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2010-05-27     Completed Date:  2010-06-25     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  9107378     Medline TA:  Biotech Histochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  267-74     Citation Subset:  IM    
Affiliation:
Department of Dental Hygiene, The Nippon Dental University College at Tokyo, Tokyo, Japan. ikedarie@tandai.ndu.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Actins / analysis
Animals
Animals, Newborn
Antibodies
Cell Differentiation
Epithelial Cells / chemistry
Epithelium / chemistry,  drug effects*
Female
Histocytochemistry
Muscle Cells / chemistry,  drug effects*
Muscle, Smooth / chemistry
Parotid Gland / chemistry,  drug effects*,  growth & development*
Proliferating Cell Nuclear Antigen / analysis
Rats
Rats, Sprague-Dawley
Secretory Vesicles / chemistry
Specific Pathogen-Free Organisms
Thyroxine / pharmacology*
Grant Support
ID/Acronym/Agency:
DE 14995/DE/NIDCR NIH HHS; R21 DE014995-02/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Actins; 0/Antibodies; 0/Proliferating Cell Nuclear Antigen; 7488-70-2/Thyroxine
Comments/Corrections
Erratum In:
Biotech Histochem. 2009 Dec;84(6):274

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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