S-Space College of Medicine/School of Medicine (의과대학/대학원) Internal Medicine (내과학전공) Journal Papers (저널논문_내과학전공)
Ghrelin enhances the proliferating effect of thyroid stimulating hormone in FRTL-5 thyroid cells
- Issue Date
- Mol Cell Endocrinol. 2008; 285 :19-25.
- Adaptor Proteins, Signal Transducing/genetics/metabolism ; Animals ; Calcium/metabolism ; Cell Line ; Cyclic AMP/metabolism ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Ghrelin/genetics/*metabolism ; Humans ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Receptors, Ghrelin/genetics/*metabolism ; STAT3 Transcription Factor/metabolism ; Shc Signaling Adaptor Proteins ; Signal Transduction/physiology ; Thyroid Gland/*cytology/metabolism ; Thyrotropin/*metabolism ; Cell Proliferation
- Ghrelin regulates cell proliferation through the growth hormone secretagogue receptor (GHS-R). We confirmed the expression of GHS-R in FRTL-5 thyroid cells and investigated the effects of ghrelin in thyrocytes using FRTL-5 cells. Ghrelin increased intracellular calcium levels but not intracellular cyclic AMP levels. Ghrelin activated Erk within 2min, then activated Akt and STAT3. Erk phosphorylation was inhibited by the calcium inhibitor cyclopiazonic acid (CPA). Ghrelin alone did not stimulate FRTL-5 cell proliferation but enhanced the effects of thyroid stimulating hormone (TSH). Pretreatment with TSH potentiates the growth effects of ghrelin in thyroid cells, and p66Shc, a growth factor receptor adaptor protein, might mediate these synergistic effects. Ghrelin phosphorylated TSH-induced p66Shc, which was inhibited by CPA. Ghrelin did not affect the proliferation of ARO cells, which showed no increased expression of p66Shc after TSH treatment. Thus, ghrelin-induced intracellular calcium signaling enhanced the TSH-induced proliferation of thyrocytes, possibly mediated by the p66Shc pathway.
- 0303-7207 (Print)
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