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VM da Costa
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DG Moreira
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D Rosenthal
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The effects of aging on human or animal thyroid function are still not well defined. We evaluated some aspects of thyroid function during aging using an animal model (young and old Dutch-Miranda rats). In old rats of both genders, serum thyroxine (T4) decreased but serum thyrotrophin (TSH) remained unaltered, suggesting a disturbance in the pituitary-thyroid feedback mechanism during aging. Serum tri-iodothyronine (T3) only decreased in old males, possibly because female rats are almost twice as efficient in hepatic T4 to T3 deiodination. Thyroidal T4-5'-deiodinase activity did not change much during aging, although it decreased slightly in males. Thyroidal iodothyronine-deiodinase type I mRNA expression but not total thyroidal enzymatic activity were higher in female than in male rats. Thus, ovarian/testicular hormones may modulate the expression and/or the activity of hepatic and thyroidal type I iodothyronine-deiodinase. Thyroperoxidase (TPO) and thyroglobulin (Tg) expression were higher in young male rats than in females. In males, TPO and Tg gene expression decreased with aging, suggesting that androgens might increase their expression. Our results showed that aging induces real changes in rat thyroid gland function and regulation, affecting at least pituitary, thyroid and liver functions. Furthermore, some of these changes were gender related, indicating that gonadal hormones may modulate thyroid gland function and regulation.

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F R S Lima
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A G Trentin
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D Rosenthal
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C Chagas
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V Moura Neto
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Abstract

Thyroid hormone (T3) induces in vitro differentiation of astrocytes from the developing rat brain. T3 treatment induced the appearance of long processes in cultured cerebral hemisphere and mesencephalon astrocytes from embryonic and newborn rats. T3 treatment also produced a change in the morphology of cultured cerebellar astrocytes from 10-day-old rats, but not in cerebellar astrocytes from newborn rats. An increased expression of glial fibrillary acidic protein (GFAP) was also seen in the T3-treated newborn cerebral hemisphere and mesencephalic astrocytes. The morphological changes were induced earlier when the astrocytes were treated with conditioned medium (CM) obtained from cultures previously exposed to T3. Our results show that astrocytes from the developing rat brain are not homogenous in their responsiveness to T3. Furthermore, the fact that CM produces a response similar to that obtained with T3 treatment but in less time, suggests that T3 might induce the secretion of factors by cultured astrocytes. These factors might, by an autocrine/paracrine effect, induce the expression of GFAP and differentiation in developing brain astrocytes.

Journal of Endocrinology (1997) 154, 167–175

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ZQ Cheng
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S Adi
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NY Wu
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D Hsiao
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EJ Woo
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EH Filvaroff
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TA Gustafson
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SM Rosenthal
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Skeletal myoblasts are inherently programmed to leave the cell cycle and begin the differentiation process following removal of exogenous growth factors. Serum withdrawal results in a marked induction of IGF production which is essential for skeletal muscle differentiation in vitro. However, the potential role of the tyrosine kinase IGF-I receptor (thought to be the principal mediator of both IGF-I and II signaling in skeletal muscle) in the decision of myoblasts to begin differentiation following serum withdrawal is unknown. To explore the role of the IGF-I receptor in this decision by skeletal myoblasts, we functionally inactivated endogenous IGF-I receptors in mouse C2C12 cells using a dominant negative, kinase-inactive IGF-I receptor in which the ATP-binding site lysine (K) at residue 1003 has been mutated to alanine (A). Cell lines with the greatest degree of mutant IGF-I receptor expression (A/K cells) demonstrated functional inactivation of endogenous IGF-I receptors as determined by their impaired ability to phosphorylate the principal substrate of the IGF-I receptor, IRS-1, in response to treatment with IGF-I. In addition, the proliferative response of myoblasts to IGF-I was completely abolished in A/K cells. Following withdrawal of exogenous growth factors, A/K cells demonstrated a marked delay in the induction of the gene expression of myogenin, a skeletal muscle-specific transcription factor essential for differentiation, and a subsequent delay in the induction of muscle creatine kinase activity. Delayed differentiation in A/K cells was associated with prolonged phosphorylation of the cell cycle regulatory retinoblastoma (Rb) protein; it is the un- (or hypo-) phosphorylated form of Rb which is known to promote differentiation in skeletal myoblasts. Thus, the IGF-I receptor regulates the timing of myoblast differentiation induced by serum withdrawal. The delayed differentiation of skeletal myoblasts with functionally inactive IGF-I receptors may result, at least in part, from delayed induction of myogenin gene expression and prolonged phosphorylation of the Rb protein.

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TG Frankenfeld
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VM Correa Da Costa
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CC Nascimento-Saba
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TM Ortiga-Carvalho
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RM Santos
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PC Lisboa
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DP Carvalho
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D Rosenthal
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Some authors have reported increased serum thyrotrophin (TSH) in animals chronically treated with lithium, suggesting that lithium might decrease pituitary thyroxine (T(4))-5'-deiodinase activity. On the other hand, the effect of lithium treatment on thyroidal T(4)-5'-deiodinase activity is also unknown. The present study was undertaken to evaluate the effects of lithium treatment on pituitary and thyroid T(4)-5'-deiodinase activity. Serum and pituitary TSH levels and thyroidal and pituitary T(4)-5'-deiodinase activities were determined in 3-month-old isogenic male Dutch-Miranda rats treated with lithium for 8 weeks. Chronic lithium treatment produced a slight increase in pituitary TSH content, but no change in serum TSH, and a significant increase in the thyroidal T(4)-5'-deiodinase activity. However, the pituitary T(4)-5'-deiodinase activity was unaffected by lithium administration. As far as we know, the present data show for the first time that chronic lithium treatment can increase the thyroxine to tri-iodothyronine conversion in the murine thyroid gland, be it directly or indirectly.

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