Transformation of Normal Follicles into Thyrotropin-Refractory “Cold” Follicles in the Aging Mouse Thyroid Gland*

Endocrinology ◽  
1978 ◽  
Vol 102 (5) ◽  
pp. 1576-1586 ◽  
Author(s):  
H. STUDER ◽  
R. FORSTER ◽  
A. CONTI ◽  
H. KOHLER ◽  
A. HAEBERLI ◽  
...  
1980 ◽  
Vol 35 (1) ◽  
pp. 3-15 ◽  
Author(s):  
H. Fujita ◽  
S. Tamura ◽  
T. Takano ◽  
S. Ishibashi ◽  
T. Tanaka

2017 ◽  
Vol 2017 ◽  
pp. 1-5
Author(s):  
Giovanna Traina ◽  
Samuela Cataldi ◽  
Paola Siccu ◽  
Elisabetta Loreti ◽  
Ivana Ferri ◽  
...  

Prevalence of thyroid dysfunction and its impact on cognition in older people has been demonstrated, but many points remain unclarified. In order to study the effect of aging on the thyroid gland, we compared the thyroid gland of very old mice with that of younger ones. We have first investigated the changes of thyroid microstructure and the possibility that molecules involved in thyroid function might be associated with structural changes. Results from this study indicate changes in the height of the thyrocytes and in the amplitude of interfollicular spaces, anomalous expression/localization of thyrotropin, thyrotropin receptor, and thyroglobulin aging. Thyrotropin and thyrotropin receptor are upregulated and are distributed inside the colloid while thyroglobulin fills the interfollicular spaces. In an approach aimed at defining the behavior of molecules that change in different physiopathological conditions of thyroid, such as galectin-3 and sphingomyelinase, we then wondered what was their behavior in the thyroid gland in aging. Importantly, in comparison with the thyroid of young animals, we have found a higher expression of galectin-3 and a delocalization of neutral sphingomyelinase in the thyroid of old animals. A possible relationship between galectin-3, neutral sphingomyelinase, and aging has been discussed.


1970 ◽  
Vol 47 (3) ◽  
pp. 333-338 ◽  
Author(s):  
PAT KENDALL-TAYLOR ◽  
D. S. MUNRO

SUMMARY The effects of dibutyryl cyclic 3′,5′-adenosine monophosphate (DBc-AMP) on the mouse thyroid gland have been investigated in the in-vitro assay of Brown & Munro (1967). The distribution of 131I-labelled compounds in the glands and the supporting medium have been analysed by thin-layer chromatography and the changes induced by cyclic 3′,5′-adenosine monophosphate (c-AMP), DBc-AMP or thyroid-stimulating hormone (TSH) compared. The release of 131I was increased when the glands were incubated with DBc-AMP, c-AMP or TSH. The potency of DBc-AMP was approximately 50 times that of c-AMP on a basis of molarity. Like TSH, DBc-AMP increased the proportion of iodothyronines in the system as a whole, whereas c-AMP had little effect. The possible explanations for this are discussed.


Science ◽  
1964 ◽  
Vol 145 (3639) ◽  
pp. 1431-1432 ◽  
Author(s):  
W. C. Bauer ◽  
J. S. Meyer

PLoS ONE ◽  
2011 ◽  
Vol 6 (2) ◽  
pp. e16752 ◽  
Author(s):  
Aurore Carre ◽  
Latif Rachdi ◽  
Elodie Tron ◽  
Bénédicte Richard ◽  
Mireille Castanet ◽  
...  

2017 ◽  
Vol 96 (5) ◽  
pp. 440-456 ◽  
Author(s):  
Jonas Weber ◽  
Joseph McInnes ◽  
Cise Kizilirmak ◽  
Maren Rehders ◽  
Maria Qatato ◽  
...  

1993 ◽  
Vol 138 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Y. Oda ◽  
K. Mashita ◽  
M. Mori-Tanaka ◽  
K. Kitajima ◽  
J. Miyagawa ◽  
...  

ABSTRACT We examined the effect of noradrenaline on the release of 3,5,3′-tri-iodothyronine (T3) and thyroxine (T4) from perifused mouse thyroid. Noradrenaline suppressed the thyrotrophin (TSH)-stimulated release of T3 and T4. The addition of prazosin, which is a specific α1 antagonist, or the depletion of Ca2+ from the perifusion buffer completely abolished the inhibitory effect of noradrenaline on TSH-stimulated T3 and T4 release. Noradrenaline did not inhibit TSH-stimulated cyclic adenosine 3′,5′-monophosphate (cAMP) release in the presence of 3-isobutyl-1-methylxanthine (IBMX), which inhibits both cAMPspecific and calmodulin-sensitive phosphodiesterases. Noradrenaline significantly suppressed the TSH-stimulated release of T3 and T4 in the presence of IBMX. These results suggest that the inhibitory effect of noradrenaline on TSH-stimulated T3 and T4 release is not mediated through a cAMP-dependent process or the activation of a calmodulin-sensitive phosphodiesterase, and that this inhibition is mediated through a Ca2+-dependent process regulated by the α1-adrenergic system in the mouse thyroid. Journal of Endocrinology (1993) 138, 73–80


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