Discordant Effects of Thyrotropin (TSH)-Releasing Hormone on Pre- and Posttranslational Regulation of TSH Biosynthesis in Rat Pituitary

Lippman, Stephen S.; Amr, Sania; Weintraub, Bruce D.

doi:10.1210/endo-119-1-343

Cited by 26 publications

(11 citation statements)

References 34 publications

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“…In conjunc tion with several lines of evidence that TRH increases tran scription rates of TSH P-and a-subunits [18] and TSH p promoter activity [19], the present data suggest that endoge nous TRH from the hypothalamus may regulate transcription rates of TSH subunits. In contrast to the present data and previous observations [7,8,18,19], it has been observed that the administration of TRH exerted little or no stimulation of rat pituitary TSH p-and a-subunit mRNA levels in either euthyroid or thyroidectomized rats [9], Therefore, the exoge nous administration of TRH may not be sufficient to increase pituitary TSH P-and a-subunit mRNA levels.…”

Section: Discussioncontrasting

confidence: 99%

“…These previous re ports indicate that TRH may stimulate TSH synthesis at the pretranslational level under certain physiological conditions. However, it has been shown that TRH had little or no activity in stimulating TSH subunit synthesis in vivo in rats [9]. Thus, the physiological role of TRH in the regulation of anterior pituitary TSH synthesis does still not reach definable conclusions.…”

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confidence: 99%

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Hypothalamic Thyrotropin-Releasing Hormone Regulates Pituitary Thyrotropin Beta- and Alpha-Subunit mRNA Levels in the Rat

Murakami¹,

Mori²,

Kato³

et al. 1991

Neuroendocrinology

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It has been controversial whether thyrotropin-releasing hormone (TRH) may be involved in the regulation of biosynthesis of anterior pituitary thyroid-stimulating hormone (TSH), whereas TRH is well known to control the secretion of TSH from anterior pituitaries. We therefore studied the effect of the destruction of paraventricular nuclei (PVN), containing TRH neuronal cell bodies, on anterior pituitary TSH β- and α-subunit mRNA levels in the thyroidectomized rat. Median eminence TRH contents and serum TSH levels significantly decreased even 1 day after PVN destruction, whereas anterior pituitary TSH β- and α-subunit mRNA levels did not change. In contrast, these mRNA levels significantly descreased by 3 days after PVN destruction. Growth hormone mRNA levels were not affected during 7 days after PVN destruction. Although the involvement of other factors related to the PVN is not totally excluded, these results raise the strong possibility that hypothalamic TRH regulates anterior pituitary TSH mRNA levels.

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Section: Discussioncontrasting

confidence: 99%

mentioning

confidence: 99%

Hypothalamic Thyrotropin-Releasing Hormone Regulates Pituitary Thyrotropin Beta- and Alpha-Subunit mRNA Levels in the Rat

Murakami¹,

Mori²,

Kato³

et al. 1991

Neuroendocrinology

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“…TRH in¬ creases TSH subunit synthesis and glycosylation (19). Although TRH can augment transcription of both TSH subunit genes in cell culture (20), it has not been shown to affect TSH subunit mRNA in the intact rat (21). Alternatively, our findings may reflect, a non-steady state in which the decrease in ß-TSH mRNA content and TSH synthesis precedes the equilibration of pituitary TSH stores.…”

Section: Discussionmentioning

confidence: 71%

Decreased anterior pituitary T3 nuclear receptors in a Walker 256 carcinoma-bearing rat model of nonthyroidal disease

Hupart

Defesi

Katz

et al. 1989

Acta Endocrinologica

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Rats bearing the Walker 256 carcinoma have decreased pituitary nuclear T3 but normal pituitary TSH content and response to experimental hypothyroidism.To elucidate further the role of T3 receptor occupancy and biological response in the tumor-bearing rat model of nonthyroidal disease, we measured the concentration of T3 nuclear receptors, rTSH and rGH and \g=b\-TSH mRNA and GH mRNA in the anterior pituitary of euthyroid rats bearing the Walker 256 carcinoma. The abundance of T3 nuclear receptors was decreased in tumorbearing rats and was associated with a decrease in mRNA content for \g=b\-TSH and GH. \g=a\-tubulinmRNA was decreased to a comparable degree. The pituitary content of rTSH and rGH was, however, the same as in control animals. Since tumor rats have normal regulation of TSH secretion by thyroid hormone, the present findings suggest that TSH secretion in T rats is maintained by a lower T3 nuclear receptor occupancy than in controls. The decrease in \g=b\-TSH mRNA may precede a decrease in TSH synthesis and changes in pituitary TSH stores. Since the decrease in GH mRNA was comparable to the decrease in \g=a\-tubulinmRNA, it does not appear to be specifically related to decreased T3 nuclear receptor occupancy. We conclude that, in the tumor-bearing rat model of nonthyroidal disease, decreases in \g=b\-TSH mRNA occur despite a decreased T3 receptor occupancy. Both thyroid-dependent and thyroid-independent factors may be involved in regulating \g=b\-TSH mRNA.Marked changes in concentration of serum thyroid hormones occur in patients with nonthyroidal dis¬ ease (1). Reports indicate that decreased concen¬ trations of serum T3 and free T3 are generally assodated with a normal serum TSH in patients with critical illness (2,3). In order to understand the bi¬ ological changes that are responsible for mainten¬ ance of a normal serum TSH in patients with de¬ creased free T3, we have previously determined the pituitary content of T3 and TSH as well as TSH regulation by thyroid hormone in euthyroid rats bearing the transplantable Walker 256 carcinoma in the thigh (4). These tumor-bearing (T) rats have been considered a good model for studies of thy¬ roid hormone action in nonthyroidal disease and experimental results employing this model have been reviewed (5). We reported that both plasma and anterior pituitary TSH were similiar in control and T rats and that plasma TSH increased simi¬ larly in both groups after induction of experimen¬ tal hypothyroidism. These findings, in association with a 50% decrease in anterior pituitary T3 con¬ tent in T rats, suggested that TSH regulation was normal in T rats but that the dose-response rela¬ tionship between pituitary T3 and TSH differed from that of control rats.Since we were unable to measure the concentra¬ tion of T3 nuclear receptors in the anterior pitui¬ tary during these studies, the relationship of these findings in T rats to the concentration of T3 recep¬ tor complexes or the fractional occupancy of T3 nuclear receptors could not be determined. In the present studi...

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“…TRH has been reported to augment TSH subunit synthesis and glycosylation (28). TSH has also been shown to increase the transcription rate of both TSH subunit genes in cell culture (29), but may not affect TSH subunit mRNAs in the intact rat (30). Earlier studies from our laboratory showed that the TRH-induced TSH release was significantly increased in T rats (9).…”

Section: Discussionmentioning

confidence: 99%

Differential Response to L-Triiodothyronine of Anterior Pituitary Growth Hormone Messenger Ribonucleic Acid (mRNA) and β-Thyrotropin mRNA in a Hypothyroid Walker 256 Carcinoma-Bearing Rat Model of Nonthyroidal Disease*

et al. 1990

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To continue our studies on the influence of T3 on TSH regulation in the Walker 256 carcinoma-bearing rat model of nonthyroidal disease, we measured the effect of T3 on pituitary content of beta TSH mRNA and rat (r) TSH in hypothyroid control (C) and tumor-bearing (T) rats. The effect of T3 on TSH regulation was compared to effects on GH mRNA and rGH in the same animals. mRNA content was normalized to a pool of pituitaries from euthyroid rats (= 1.0). beta TSH mRNA increased 18-fold in both hypothyroid C and T rats and then decreased similarly with increasing T3 infusion to a value of 0.1. GH mRNA content decreased to 0.11 +/- 0.01 in hypothyroid C rats, but to only 0.38 +/- 0.02 in T rats (P less than 0.001). The pituitary contents of GH mRNA and rGH in hypothyroid T rats was significantly greater than those in C rats at all T3 infusion rates. These data together with our previous report of decreased nuclear T3 in T rats suggest that regulation of beta TSH mRNA by T3 is intact in T rats, but occurs at a lower concentration of nuclear T3. In contrast, the GH mRNA response is enhanced, displaying differential regulation of these two T3-responsive gene products in this model of nonthyroidal illness.

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Discordant Effects of Thyrotropin (TSH)-Releasing Hormone on Pre- and Posttranslational Regulation of TSH Biosynthesis in Rat Pituitary

Cited by 26 publications

References 34 publications

Hypothalamic Thyrotropin-Releasing Hormone Regulates Pituitary Thyrotropin Beta- and Alpha-Subunit mRNA Levels in the Rat

Hypothalamic Thyrotropin-Releasing Hormone Regulates Pituitary Thyrotropin Beta- and Alpha-Subunit mRNA Levels in the Rat

Decreased anterior pituitary T3 nuclear receptors in a Walker 256 carcinoma-bearing rat model of nonthyroidal disease

Differential Response to L-Triiodothyronine of Anterior Pituitary Growth Hormone Messenger Ribonucleic Acid (mRNA) and β-Thyrotropin mRNA in a Hypothyroid Walker 256 Carcinoma-Bearing Rat Model of Nonthyroidal Disease*

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