The in Vitro Effects of Thyroid-Stimulating Hormone and Thyroid-Stimulating Immunoglobulins on Human Thyroid Membrane Adenylate Cyclase or Cyclic Amp Accumulation in Thyroid Slices

1978 ◽  
Vol 54 (2) ◽  
pp. 35P-36P
Author(s):  
S. Holmes ◽  
T. J. Martin ◽  
Susan Dirmikis ◽  
D. S. Munro
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Thyroid Stimulating Hormone ◽  
Human Thyroid ◽  
Thyroid Stimulating Immunoglobulins ◽  
Cyclic Amp Accumulation ◽  
In Vitro Effects ◽  
Stimulating Hormone

EFFECTS OF HUMAN THYROID-STIMULATING HORMONE AND IMMUNOGLOBULINS ON ADENYLATE CYCLASE ACTIVITY AND THE ACCUMULATION OF CYCLIC AMP IN HUMAN THYROID MEMBRANES AND SLICES

1978 ◽  
Vol 79 (1) ◽  
pp. 121-130 ◽  
Author(s):  
S. D. HOLMES ◽  
SUSAN M. DIRMIKIS ◽  
T. J. MARTIN ◽  
D. S. MUNRO
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Thyroid Stimulating Hormone ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Maximum Response ◽  
Human Thyroid ◽  
Tissue Slices ◽  
Long Acting ◽  
Stimulating Hormone

The activation of adenylate cyclase and the accumulation of cyclic AMP resulting from the action of human thyroid-stimulating hormone (TSH), long-acting thyroid stimulator (LATS) or LATS-protector (LATS-P) have been investigated in preparations of human thyroid membranes and slices. Human TSH significantly increased adenylate cyclase activity in membranes from non-toxic goitres whereas LATS and LATS-P had no consistent effect. However, pre-incubation of goitrous membranes with LATS–immunoglobulin G inhibited the effect of TSH on adenylate cyclase. When thyroid membranes were prepared from the glands of patients with Graves's disease neither TSH nor thyroid-stimulating immunoglobulins (TSIg) stimulated adenylate cyclase significantly. Whether from non-toxic goitres or thyrotoxic tissue, the concentration of TSH needed to induce half of the maximum response was lower in thyroid slices than in membranes. Both LATS and LATS-P significantly stimulated the accumulation of cyclic AMP in slices of goitrous tissue but thyrotoxic tissue slices did not respond. In goitrous slices, submaximum concentrations of TSH and TSIg caused additive responses in the accumulation of cyclic AMP but TSIg did not increase the maximum response to TSH.

scholarly journals Hipotiroidismo Associado a Anticorpos Anti-Receptor da Hormona TSH com Ação Bloqueadora Determinada In Vitro

2015 ◽  
Vol 28 (5) ◽  
pp. 663
Author(s):  
Pedro Marques ◽  
Karim Chikh ◽  
Anne Charrié ◽  
Rosa Pina ◽  
Maria João Bugalho ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Thyroid Stimulating Hormone ◽  
Human Thyroid ◽  
In Vitro Tests ◽  
Lymphocytic Thyroiditis ◽  
Blocking Activity ◽  
Stimulating Hormone

Thyroid-stimulating hormone-receptor autoantibodies normally causes hyperthyroidism. However, they might have blocking activity causing hypothyroidism. A 11-year-old girl followed due to type 1 diabetes mellitus, celiac disease and euthyroid lymphocytic thyroiditis at diagnosis. Two years after the initial evaluation, thyroid-stimulating hormone was suppressed with normal free T4; nine months later, a biochemical evolution to hypothyroidism with thyroid-stimulating hormone-receptor autoantibodies elevation was seen; the patient remained always asymptomatic. Chinese hamster ovary cells were transfected with the recombinant human thyroid-stimulating hormone -receptor, and then exposed to the patient´s serum; it was estimated a ‘moderate’ blocking activity of these thyroid-stimulating hormone-receptor autoantibodies, and concomitantly excluded stimulating action. In this case, the acknowledgment of the blocking activity of the serum thyroid-stimulating hormone-receptor autoantibodies, supported the hypothesis of a multifactorial aetiology of the hypothyroidism, which in the absence of the in vitro tests, we would consider only as a consequence of the destructive process associated to lymphocytic thyroiditis.

Renal cyclic AMP accumulation and adenulate cyclase stimulation by erythropoietic agents

1975 ◽  
Vol 229 (5) ◽  
pp. 1387-1392 ◽  
Author(s):  
GM Rodgers ◽  
JW Fisher ◽  
WJ George
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Regional Distribution ◽  
Renal Medulla ◽  
Iron Incorporation ◽  
Erythropoietin Production ◽  
Cyclic Amp Accumulation ◽  
Stimulation Of

The regional distribution of cyclic AMP in the kidney was determined following erythropoietic stimulation with hypoxia and cobalt. Following these stimuli, increases in renal cyclic AMP concentrations were restricted to the cortex. The basis for this localization in the case of cobalt treatment was found to reside in the stimulation of renal cortical adenylate cyclase activity in vitro by concentrations of cobalt similar to those found in vivo. The level of cobalt in the cortex after cobalt treatment was found to approach 500 mumol/kg of tissue, whereas no detectable levels of cobalt were found in the renal medulla. Additionally, other agents such as parathyroid hormone and lactic acid, that are known to lack stimulatory effects on medullary adenylate cyclase, were found to stimulate the cortical enzyme. This stimulation of renal cortical adenylate cyclase correlates with enhanced erythropoiesis as demonstrated by increased radiolabeled iron incorporation into erythrocytes. These results support previous reports which suggest that renal cortical cyclic AMP mediates erythropoietin production in response to erythropoietically active agents.

A COMPARISON OF THE IN-VITRO ACTIONS OF THYROID-STIMULATING HORMONE AND CYCLIC 3′,5′-ADENOSINE MONOPHOSPHATE ON THE MOUSE THYROID GLAND

1969 ◽  
Vol 43 (3) ◽  
pp. 477-485 ◽  
Author(s):  
JANICE M. ENSOR ◽  
D. S. MUNRO
Keyword(s):  
Cyclic Amp ◽  
Culture Medium ◽  
Adenosine Monophosphate ◽  
Thyroid Stimulating Hormone ◽  
Vitro Assay ◽  
Thyroid Glands ◽  
Influence Of Tsh ◽  
Mouse Thyroid ◽  
Stimulating Hormone

SUMMARY In the in-vitro assay of Brown & Munro (1967) thyroid-stimulating hormone (TSH) increased the release of radioactive iodine from mouse thyroid glands labelled with 131i during life. Paper chromatography showed that TSH increased the 131I-labelling of thyroxine and tri-iodothyronine both in the culture medium and in hydrolysates of the thyroids. Cyclic 3′,5′-adenosine monophosphate (cyclic AMP) also increased 131I release in this assay and increased the 131I-labelling of thyronines in the culture medium. The effects on thyroid hydrolysates were less striking. Theophylline potentiated the influence of TSH and cyclic AMP in the assay and, by itself, increased 131I release and the labelling of iodothyronines in the thyroid without altering the distribution of 131I in the culture medium. The implications of these results are discussed.

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