Regulation by thyroid status of c-myc, c-fos and H-ras mRNAs in the rat myocardium

1991 ◽  
Vol 130 (2) ◽  
pp. 239-244 ◽  
Author(s):  
N. K. Green ◽  
M. D. Gammage ◽  
J. A. Franklyn ◽  
M. C. Sheppard
Keyword(s):  
Protein Synthesis ◽  
Thyroid Hormones ◽  
Contractile Protein ◽  
Rat Myocardium ◽  
Direct Effects ◽  
Thyroid Status ◽  
Critical Signal ◽  
Ras Genes ◽  
Intracellular Signals ◽  
Oncogene Products

ABSTRACT Effects of thyroid status on expression of a variety of myocardial genes, such as those encoding contractile proteins, have been reported, as well as interactions between thyroid hormones and developmental and haemodynamic regulation of contractile protein synthesis. In addition, it is clear that developmental and haemodynamic factors regulate expression of specific proto-oncogenes, including c-myc, c-fos and H-ras, in the myocardium but the effect of thyroid status on such proto-oncogene products, which are proposed to play a critical signal-transducing role in the heart, has been previously unexplored. In order to determine whether changes in thyroid status are associated with changes in expression of these putative intracellular signals, we examined the effect of hypothyroidism and tri-iodothyronine (T3) treatment on myocardial levels of c-myc, c-fos and H-ras mRNAs in the rat. The induction of hypothyroidism was associated with a marked increase in myocardial c-myc, c-fos and H-ras mRNAs, changes reversed by 72 h of T3 replacement. Administration of T3 to euthyroid rats had no significant effect on myocardial c-myc or c-fos mRNAs, but inhibition of H-ras mRNA by T3 was evident. These observations demonstrating influences of thyroid status on expression of specific proto-oncogenes suggest that thyroid hormones, as well as exerting direct effects on expression of functionally important myocardial genes, also interact with the cellular transduction pathways mediated by the products of the c-myc, c-fos and H-ras genes. Journal of Endocrinology (1991) 130, 239–244

scholarly journals Stress and thyroid gland

2010 ◽  
Vol 56 (4) ◽  
pp. 443-456 ◽  
Author(s):  
L.I. Nadolnik
Keyword(s):  
Thyroid Hormones ◽  
The Body ◽  
Direct Effects ◽  
Thyroid Status ◽  
Acute And Chronic Stress ◽  
Adrenal System ◽  
Thyroid Metabolism ◽  
Peripheral Metabolism ◽  
Different Tissues

The review highlights the effects of acute and chronic stress on thyroid metabolism. Special attention is paid to the influence of stress and the direct effects of glucocorticoids on the thyroid status, the activities of thyrocyte iodine uptake, oxidation and organification as well as peripheral metabolism of thyroid hormones (deposition and transport of thyroid hormones, deiodinase activities in different tissues). The role of stress in the development of thyroid pathology is analysed and charestiristic features of thyroid function alterations during impaired functioning of the pitiutary-adrenal system are established. The mechanisms of the stress-induced impairments in thyroid functions are of interest for further research, taking into consideration serious consequences of thyroid deficiency for the body, even in subclinical thyroid insufficiency.

Direct anabolic effects of thyroid hormone on isolated mouse heart

1983 ◽  
Vol 245 (5) ◽  
pp. C328-C333 ◽  
Author(s):  
J. S. Crie ◽  
J. R. Wakeland ◽  
B. A. Mayhew ◽  
K. Wildenthal
Keyword(s):  
Protein Synthesis ◽  
Thyroid Hormones ◽  
Protein Degradation ◽  
Mouse Heart ◽  
Direct Effects ◽  
Systemic Hemodynamic ◽  
Isolated Hearts ◽  
Beating Rate ◽  
Small Inhibition

The direct effects of L-and D-triiodothyronine (T3) on cardiac protein metabolism were investigated using fetal mouse hearts in organ culture. This model allowed the production of "thyrotoxicosis" in isolated hearts in vitro in the absence of the usual systemic metabolic and hemodynamic effects of thyroid hormones. Hearts were studied during the first 24 h of T3 exposure in culture, before changes in beating rate due to T3 occurred. Phenylalanine release was decreased by 26 +/- 2.3% (P less than 0.001) by the optimal concentrations of T3 (10(-7) to 10(-6) M). Changes were similar in the presence or absence of insulin. D-T3 was also anabolic, decreasing phenylalanine release by 24 +/- 2.5% (P less than 0.001) at concentrations of 10(-6) to 10(-5) M. The L-isomer increased protein synthesis by 23 +/- 6.8% (P less than 0.05) and decreased protein degradation, as measured by phenylalanine release in the presence of cycloheximide, by 5 +/- 1.6% (P less than 0.01). The D-isomer also increased protein synthesis but had no measurable effect on protein degradation. We conclude that thyroid hormones can exert direct anabolic effects on heart in the absence of systemic hemodynamic and metabolic changes. These effects are mediated primarily through an acceleration of the rate of protein synthesis; in the case of L-T3, a small inhibition of proteolysis may also occur.

Muscle dedifferentiation and contractile protein synthesis during post-traumatic regeneration by Owenia fusiformis (polychaete annelid)

1983 ◽  
Vol 13 (4) ◽  
pp. 267-282 ◽  
Author(s):  
Michel Fontés ◽  
Josiane Coulon ◽  
Marie-Hélène Delgross ◽  
Yves Thouveny
Keyword(s):  
Protein Synthesis ◽  
Contractile Protein ◽  
Post Traumatic

Profoundly lower muscle mass and rate of contractile protein synthesis in boys with Duchenne muscular dystrophy

2021 ◽  
Author(s):  
William J. Evans ◽  
Mahalakshmi Shankaran ◽  
Edward C. Smith ◽  
Carl Morris ◽  
Edna Nyangau ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Muscle Mass ◽  
Contractile Protein

scholarly journals Na,K-ATPase mRNAbeta1 expression in rat myocardium - effect of thyroid status

1999 ◽  
Vol 260 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Yvonne Shao ◽  
Thomas A. Pressley ◽  
Faramarz Ismail-Beigi
Keyword(s):  
Rat Myocardium ◽  
Thyroid Status

Maternal Thyroid Status and the Incidence of Respiratory Distress Syndrome: Evaluation of a Proposed Relationship

PEDIATRICS ◽  
1975 ◽  
Vol 55 (4) ◽  
pp. 497-499
Author(s):  
Richard M. Cowett ◽  
Leo Stern
Keyword(s):  
Thyroid Hormones ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Retrospective Analysis ◽  
Low Birthweight ◽  
Distress Syndrome ◽  
Thyroid Status ◽  
Thyroid Activity ◽  
Fetal Thyroid ◽  
Maternal Thyroid

In order to establish whether maternal thyroid hormones cross the placenta and produce surfactant in the fetus, possibly reducing the incidence of respiratory distress syndrome (RDS), a retrospective analysis of low-birthweight infants was undertaken. Results indicate that maternal thyroid hormones play a negligible role and that any thyroid mediation would result from fetal thyroid activity.

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