scholarly journals Antagonistic effects of thyrotropin and epidermal growth factor on thyroglobulin mRNA level in cultured thyroid cells

1985 ◽  
Vol 152 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Pierre P. ROGER ◽  
Brigitte HEUVERSWYN ◽  
Christine LAMBERT ◽  
Sylvia REUSE ◽  
Gilbert VASSART ◽  
...  
1993 ◽  
Vol 265 (2) ◽  
pp. E323-E331 ◽  
Author(s):  
H. Kurachi ◽  
H. Adachi ◽  
S. Ohtsuka ◽  
K. Morishige ◽  
K. Amemiya ◽  
...  

Ovariectomy (Ovx) of mice significantly increases the epidermal growth factor (EGF) concentration in the submandibular gland. To elucidate the role of this elevated EGF in obesity of Ovx mice, we examined the effects of sialoadenectomy (Sx) and anti-EGF rabbit antiserum administration on the body weight (BW) gain and carcass fat deposition in Ovx animals. Studies were performed in four groups of mice consisting of control, Ovx, Ovx+Sx, and Ovx+anti-EGF groups. Ovx increased the BW gain compared with the control animals, whereas Sx and anti-EGF significantly reduced it. Although the relative weights (weight ratio to BW) of the liver and kidney were not significantly changed by Ovx, Sx, or anti-EGF treatment of Ovx mice, the relative weights of mesenteric, parametrial, and subcutaneous fat tissues were increased in Ovx mice, and this increase was significantly reduced by Sx or anti-EGF administration. Ovx induced adipocyte hypertrophy, and this effect was eliminated by Sx and anti-EGF. Moreover, acyl-CoA synthetase mRNA level was increased by Ovx, and this increase was reduced by Sx and anti-EGF in mesenteric fat tissue. These findings suggest that elevation of EGF may play a role in the induction of obesity in Ovx mice.


1986 ◽  
Vol 22 (1) ◽  
pp. 28-36 ◽  
Author(s):  
Janice E. Errick ◽  
Katherine W. A. Ing ◽  
Margaret C. Eggo ◽  
Gerard N. Burrow

Thyroid ◽  
1992 ◽  
Vol 2 (3) ◽  
pp. 181-187 ◽  
Author(s):  
YUEH-CHU L. TSENG ◽  
KENNETH D. BURMAN ◽  
SABITA LAHIRI ◽  
JUAN D'AVIS ◽  
LEONARD WARTOFSKY

1987 ◽  
Vol 114 (2) ◽  
pp. 179-184 ◽  
Author(s):  
S. Atkinson ◽  
P. Kendall-Taylor

ABSTRACT Primary cultures of porcine thyroid cells, grown as monolayers, showed saturable binding of epidermal growth factor (EGF). Scatchard analysis resolved the binding to a high-affinity/low-capacity site (dissociation constant = 0·17 nmol/l, maximal binding capacity = 1·67 pmol/106 cells) and a low-affinity/high-capacity site. Preincubation of thyroid monolayers with TSH for 3 days caused an increase in binding of 125I-labelled EGF due to an increase in the number of receptors, with the binding affinity unchanged. This effect was dose-dependent within the range of TSH concentrations 0·01–100 mu/l. The same effect was seen with dibutyryl cyclic AMP (10–1000 μmol/l). When the protein synthesis inhibitor cycloheximide was included in the TSH preincubation, the increase in EGF binding was abolished. The TSH effect on EGF binding was not mediated by thyroid hormones, since neither thyroxine (T4) nor tri-iodothyronine (T3) at 01 nmol/l–10 μmol/l could mimic the effect of TSH, nor could antisera to T3 or T4 neutralize the effect of TSH. The concentration of extracellular iodide (10 nmol/l–10 mmol/l) had no effect on the binding of 125I-labelled EGF. The results demonstrate that TSH increases the number of receptor sites for binding of EGF to thyroid monolayers in vitro. This effect is dependent upon protein synthesis and is mediated by cyclic AMP but not by thyroid hormones or iodide. This effect on binding of EGF may contribute to the trophic action of TSH. J. Endocr. (1987) 114, 179–184


1987 ◽  
Vol 49 (2-3) ◽  
pp. 109-117 ◽  
Author(s):  
M.J. Waters ◽  
R.C. Tweedale ◽  
T.A. Whip ◽  
G. Shaw ◽  
S.W. Manley ◽  
...  

1995 ◽  
Vol 15 (1) ◽  
pp. 73-79 ◽  
Author(s):  
T Monden ◽  
M Yamada ◽  
S Konaka ◽  
T Satoh ◽  
H Ezawa ◽  
...  

ABSTRACT To gain insight into the mechanism underlying the epidermal growth factor (EGF)-induced changes in responsiveness to TRH and in the numbers of TRH receptors (TRH-Rs) in the pituitary, we investigated the transcriptional regulation by EGF of the TRH-R gene in GH4C1 cells. Northern blot analyses and binding studies revealed that EGF reduced both TRH binding and TRH-R mRNA levels in a dose- and time-dependent manner, while no significant changes were observed in β-actin mRNA levels. Addition of actinomycin D caused an acute increase in the basal TRH-R mRNA level, and the rate of decrease of the TRH-R mRNA was identical in control and EGF-treated groups, suggesting that the stability of the TRH-R mRNA was not significantly affected in EGF-treated cells. Incubation with cycloheximide also induced an increase in the basal TRH-R mRNA level and completely reversed the EGF-induced reduction of TRH-R mRNA levels. Furthermore, a nuclear run-on assay demonstrated that the rate of transcription of the TRH-R gene was significantly inhibited in cells treated with EGF. We conclude that (1) EGF decreases the expression of the TRH-R mRNA largely by reducing its rate of transcription, and this action requires the synthesis of new proteins, and (2) inhibitors of protein and RNA synthesis cause a significant increase in the basal TRH-R mRNA level, suggesting that there may be a short-lived protein suppressing the TRH-R mRNA level in the pituitary.


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