Thyroid hormone regulation of Na,K-ATPase subunit-mRNA expression in neonatal rat myocardium

The mechano growth factor (MGF), a splice variant of the IGF-I gene, was first discovered in mechanically overloaded skeletal muscle and was shown to play an important role in proliferation of muscle stem cells. Since then, the presence and effects of MGF have been demonstrated in other tissues. MGF has been shown to act neuroprotectively during brain ischemia, and pretreatment with MGF before myocardial infarction improves cardiac function. Because MGF plays a permissive role in exercise-induced skeletal muscle hypertrophy, we hypothesize that MGF is commonly involved in cardiac hypertrophy. To investigate the regulation of MGF expression in heart, mice were treated with thyroid hormone (T3) for 12 d to induce physiological cardiac hypertrophy. MGF mRNA expression was specifically increased in midregions of the septum and left ventricular wall. Interestingly, MGF expression strongly correlated with the increased or decreased beating frequency of hyperthyroid and hypothyroid hearts. To further investigate the mechanically dependent induction of MGF, neonatal rat cardiomyocytes were isolated and exposed to T3. Upon T3 treatment, cardiomyocytes increased both contractile activity measured as beats per minute and MGF as well as IGF-IEa mRNA expression. Importantly, when cardiomyocytes were contractile arrested by KCl, simultaneous exposure to T3 prevented the up-regulation of MGF, whereas IGF-IEa was still induced. These studies demonstrated that MGF but not IGF-IEa expression is dependent on beating activity. These findings suggest that MGF is specifically stimulated by mechanical loading of the heart to mediate the hypertrophic response to thyroid hormone.

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Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

Journal of Endocrinology ◽

10.1677/joe-07-0253 ◽

2007 ◽

Vol 195 (3) ◽

pp. 429-438 ◽

Cited By ~ 11

Author(s):

C R Liu ◽

L Y Li ◽

F Shi ◽

X Y Zang ◽

Y M Liu ◽

...

Keyword(s):

Thyroid Hormone ◽

Mrna Expression ◽

Hormone Receptor ◽

Thyroid Hormone Receptor ◽

Developmental Process ◽

Control Group ◽

Rat Myocardium ◽

Receptor Mrna ◽

Close Relationship ◽

Heart Lesions

Thyroid dysfunction is classified into hyperthyroidism and congenital hypothyroidism (CH). Both hyperthyroidism and CH can cause heart lesions; however, the mechanisms involved remain unclear. The left ventricle was collected from eu-, hyper-, and hypothyroid rat. RNA was extracted and reverse-transcripted to cDNA. Real-time fluorescence quantitation-PCR was used to quantify the differential expression of thyroid hormone receptor (TR) subtype mRNA among eu-, hyper-, and hypothyroid rat myocardium. Here, we show that compared with the normal myocardium, TRα1 mRNA expression was upregulated by 51% (P<0.01), TRα2 mRNA expression was downregulated by 58% (P<0.01), and TRβ1 mRNA expression remained unchanged in hyperthyroid rat myocardium (P>0.05). TRα1, TRα2, and TRβ1 were expressed in normal and hypothyroid rat myocardium throughout the developmental process. In hypothyroid rats, myocardial TRα1 mRNA expression was generally downregulated and the expression peak appeared late. Myocardial TRα2 mRNA expression was generally upregulated and the expression peak appeared late. Myocardial TRβ1 mRNA expression was generally downregulated and changed similarly with the control group. In addition, the hypogenetic myocardium can be seen in the hypothyroid rat by pathology study. Taken together, the abnormal expression of TR subtype mRNA may have a close relationship with the pathogenesis of CH and hyperthyroidism heart disease.

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Follicle-stimulating hormone regulation of inhibin α-subunit mRNA in staged rat seminiferous tubules

Acta Endocrinologica ◽

10.1530/eje.0.1310323 ◽

1994 ◽

Vol 131 (3) ◽

pp. 323-329 ◽

Cited By ~ 4

Author(s):

Antti Kaipia ◽

Tarja-Leena Penttilä ◽

Jorma Toppari

Keyword(s):

Mrna Expression ◽

Hormonal Regulation ◽

Mrna Level ◽

Follicle Stimulating Hormone ◽

Seminiferous Tubules ◽

Mrna Levels ◽

Hormone Regulation ◽

Α Subunit ◽

Subunit Mrna ◽

Stimulating Hormone

Kaipia A, Penttilä T-L, ToppariJ. Follicle-stimulating hormone regulation of inhibin α-subunit mRNA in staged rat seminiferous tubules. Eur J Endocrinol 1994;131:323–9. ISSN 0804–4643 Steady-state levels of inhibin-α and -βB mRNAs are higher in stages II–VI of the seminiferous epithelial cycle than in stages VII–VIII We investigated follicle-stimulating hormone (FSH) regulation of inhibin α-subunit mRNA in stages II–VI and VII–VIII to study whether the stage specificity is due to differential hormonal regulation by FSH. Follicle-stimulating hormone caused a significant increase of inhibin-α mRNA levels in both stages during a 20-h incubation. The mechanism of the FSH effect was studied further in stages VII-VIII. Maximal stimulation of the inhibin-α mRNA level was achieved with 100 μg/l FSH, dibutyryl-3′,5′-cyclic adenosine monophosphate (db-cAMP, 0.2 mmol/l) and Spadenosine-3′,5′-monophosphothionate (Sp-cAMPS, 10 μmol/l) (a cAMP agonist). The presence of RpcAMPS (200 μmol/l) (a cAMP antagonist) abolished the stimulation, Rp-cAMPS alone had no effect. inhibin-βB mRNA levels in stages VII–VIII were not affected by FSH, db-cAMP, Sp-cAMPS or Rp-cAMPS. Phorbol 12-myristate 13-acetate (100 nmol/l) had no effect on inhibin-α or -βB mRNA levels. Actinomycin D abolished the stimulatory effect of FSH on inhibin-α mRNA expression. In conclusion, FSH stimulated inhibin-α mRNA expression similarly both in stages II–VI and VII–VIII of the seminiferous epithelial cycle and the stimulation in stages VII–VIII was cAMP-mediated. Jorma Toppari, University of Turku, Institute of Biomedicine, Department of Physiology, Kiinamyllynkatu 10, FIN-20520 Turku, Finland

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Expression and thyroid hormone regulation of annexins in the anterior pituitary

Journal of Endocrinology ◽

10.1677/joe-07-0042 ◽

2007 ◽

Vol 195 (3) ◽

pp. 385-392 ◽

Cited By ~ 7

Author(s):

Jens Mittag ◽

Wiebke Oehr ◽

Heike Heuer ◽

Tuula Hämäläinen ◽

Bent Brachvogel ◽

...

Keyword(s):

Thyroid Hormone ◽

Mrna Expression ◽

Hormone Secretion ◽

Pituitary Hormones ◽

Pituitary Hormone ◽

Dependent Manner ◽

Hormone Regulation ◽

Wild Type ◽

Transcript Levels ◽

Redundant Functions

Due to their property to bind to phospholipids in a Ca2+-dependent manner, proteins of the annexin superfamily are involved in many membrane-related events and thus in various forms of physiological and pathological processes. We were therefore interested in analyzing the mRNA expression of the annexins in the severely disorganized pituitaries of the athyroid Pax8−/− mice in comparison with that of control animals. In neither condition was mRNA expression of the annexins A3, A7, A8, A9, A11, and A13 detectable. The annexins A2, A4, and A6 were equally expressed in wild-type and Pax8−/− mice. Transcript levels of A1 and A10 were highly increased and those of A5 were significantly decreased in the athyroid mutants compared with controls. Treatment of Pax8−/− mice with physiological doses of thyroxine for 3 days normalized the mRNA expression of A1, A5, and A10 indicating that the expression of these annexins is directly regulated by thyroid hormone (TH). Since A5 exhibits by far the highest transcript levels of all annexins in the pituitary and its regulation by TH could be also confirmed at the protein level, we analyzed the mRNA expression of pituitary hormones in A5−/− mice. In these mutants, only the β-FSH mRNA expression was found to be significantly reduced, while the mRNA expression levels of the other pituitary hormones were not altered. These results support the concept that annexins might serve important albeit redundant functions as modulators of pituitary hormone secretion.

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