Document Detail

Thyrotropin prevents apoptosis by promoting cell adhesion and cell cycle progression in FRTL-5 cells.
MedLine Citation:
PMID:  10579364     Owner:  NLM     Status:  MEDLINE    
Apoptosis has been shown to be involved in endocrine tissue homeostasis as well as regression due to hormone deprivation. The goal of this study was to induce apoptosis and to investigate a potential role of TSH as a survival factor in thyroid follicular cells (FRTL-5) in vitro. Our results indicated that FRTL-5 cells underwent anchorage-dependent apoptosis when plated in the absence of serum and hormones, but when the cells became attached to the substrate by addition of TSH in the medium, apoptosis was prevented. The apoptosis was evaluated by positive terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling staining, typical apoptotic bodies by electron microscopy, DNA ladder by gel electrophoresis, and subdiploidy by propidium iodide-stained flow cytometry. TSH was shown to prevent apoptosis and maintain cell viability. cAMP partly mimicked this effect, which was inhibited by a specific inhibitor of protein kinase A, H-89. While investigating the mechanisms of apoptosis, we observed that the phosphorylated focal adhesion kinase was strengthened by TSH. Furthermore, FRTL-5 cells were found to undergo growth arrest in the G1 phase in the absence of TSH, accompanied by an elevated level of cyclin-dependent kinase inhibitor, p27, and a decreased level of cyclin D. In contrast, TSH promoted transition from G1 to S phase by decreasing P27 protein and increasing cyclin D expression. We concluded that in addition to regulating growth and differentiation, TSH may function as a survival factor in thyroid cells by preventing anchorage-dependent apoptosis in FRTL-5 cells partly via the cAMP pathway.
X Li; S Lu; E Miyagi; R Katoh; A Kawaoi
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Endocrinology     Volume:  140     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1999 Dec 
Date Detail:
Created Date:  1999-12-20     Completed Date:  1999-12-20     Revised Date:  2012-06-05    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  5962-70     Citation Subset:  AIM; IM    
Department of Pathology, Yamanashi Medical University, Nakakoma, Japan.
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MeSH Terms
Apoptosis / drug effects*
Blotting, Western
Cell Adhesion / drug effects*
Cell Adhesion Molecules / analysis,  metabolism
Cell Cycle / drug effects*
Cell Line
Culture Media, Serum-Free
DNA Fragmentation
Flow Cytometry
Fluorescent Antibody Technique, Indirect
Focal Adhesion Kinase 1
Focal Adhesion Protein-Tyrosine Kinases
G1 Phase / drug effects
In Situ Nick-End Labeling
Microscopy, Electron
Protein-Tyrosine Kinases / metabolism
S Phase / drug effects
Thyroid Gland / cytology*
Thyrotropin / administration & dosage,  pharmacology*
Reg. No./Substance:
0/Cell Adhesion Molecules; 0/Culture Media, Serum-Free; 9002-71-5/Thyrotropin; EC Adhesion Kinase 1; EC Kinases; EC Adhesion Protein-Tyrosine Kinases; EC protein, rat

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