Synergistic transcriptional activation of the thyrotropin receptor promoter by cyclic AMP-responsive-element-binding protein and thyroid transcription factor 1

Saiardi, Adolfo; Falasca, P.; Civitareale, Donato

doi:10.1042/bj3100491

Cited by 12 publications

(4 citation statements)

References 34 publications

(53 reference statements)

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“…Again, the promoter elements identified presently, which include binding sites for thyroid hormone receptor (TR)-α1/retinoid-X receptor (RXR) heterodimer, 229 GAbinding protein (GABP), 230 cAMP responsive element binding (CREB) protein, 231 and TTF-1 232 (see Fig. 75-7), do not display a clear thyroid-specific activity in transfection experiments, as could be expected.…”

Section: Thyrotropin Receptormentioning

confidence: 73%

Thyroid Regulatory Factors

Dumont¹,

Maenhaut²,

Christophe³

et al. 2016

Endocrinology: Adult and Pediatric

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Section: Thyrotropin Receptormentioning

confidence: 73%

Thyroid Regulatory Factors

Dumont¹,

Maenhaut²,

Christophe³

et al. 2016

Endocrinology: Adult and Pediatric

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“…3A). Interestingly, a functional cAMP-response element between Ϫ139 and Ϫ131 bp upstream of the translational initiation site of the human TSHR gene has also been characterized and is known to be conserved in mammals (30). It is known that an increase in gonadotropins will stimulate follicle growth and luteinization, which is accompanied by a significant increase in the estradiol level.…”

Section: Discussionmentioning

confidence: 99%

Thyrostimulin, but Not Thyroid-stimulating Hormone (TSH), Acts as a Paracrine Regulator to Activate the TSH Receptor in Mammalian Ovary

Sun¹,

Hsu²,

Wu³

et al. 2010

Journal of Biological Chemistry

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The thyroid-stimulating hormone receptor (TSHR), activated by either TSH or the newly discovered glycoprotein hormone thyrostimulin, plays a central role in the control of body metabolism. Interestingly, in addition to its thyroid expression, we discovered that the mRNA level of TSHR is periodically regulated in rat ovary by gonadotropins. Ovarian microdissection followed by real-time PCR analysis indicated that granulosa cells show the highest level of TSHR expression. Cultures of follicles and primary granulosa cells demonstrated that the level of TSHR is up-regulated and decreased by the gonadotropindriven cAMP cascade and estradiol production, respectively. Furthermore, in contrast to the negligible expression of TSH in the ovary, we also found by real-time PCR and immunohistochemical analysis that thyrostimulin is expressed mainly in oocytes. Evolving before the appearance of gonadotropins, thyrostimulin is considered the most ancestral glycoprotein hormone. Therefore, the presence of thyrostimulin in the ovary suggests that it may have a primitive function in reproduction when it activates ovarian TSHR. Next, we generated recombinant thyrostimulin protein and characterized its non-covalent heterodimeric nature. Using purified recombinant thyrostimulin, we show that the human ovarian cell line NIH:OVCAR-3 also expresses endogenous and functional TSHR. Using cultured rat granulosa cells isolated from different ovarian stages, we found that treatments with thyrostimulin significantly increase cAMP production and the c-fos gene response in the presence of gonadotropins. Thus, this study demonstrates that oocyte-derived thyrostimulin and granulosa cell-expressed TSHR compose a novel paracrine system in the ovary, where the activity is tightly controlled by gonadotropins.

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“…In the T1␣ promoter, this putative binding site is juxtaposed to the TTF-1 binding region and, in the SP-B promoter, to the HNF-3 site adjacent to the TTF-1 sites. Synergistic transcriptional activation of several promoters by CREB and other cell-specific transcription factors has been reported (67). For example, cooperativity of TTF-1 and CREB is important for activation of the thyrotropin receptor promoter, enhancing expression about 20-fold.…”

Section: Table I Sequences Of the Oligonucleotides Used In The Electrmentioning

confidence: 99%

TGT3, Thyroid Transcription Factor I, and Sp1 Elements Regulate Transcriptional Activity of the 1.3-Kilobase Pair Promoter ofT1α, a Lung Alveolar Type I Cell Gene

Ramirez

Rishi

Cao

et al. 1997

Journal of Biological Chemistry

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The alveolar type I epithelial cell forms the major cellular surface (ϳ70 m 2 , human) for gas exchange in the mammalian lung. Despite this important function, very little is known about its molecular phenotype or regulation of expression of its cell-specific genes (1). We have recently cloned, sequenced, and characterized a gene, T1␣, that we believe is the first definitive marker for this cell type in the adult rat lung (2, 3). The gene encodes an apical transmembrane protein that is expressed by type I cells but not by adjacent alveolar epithelial type II cells.Characterizing the regulation of this new marker for the type I cell phenotype is likely to be important for understanding the general processes by which type I cells differ in gene regulation, structure, and biology from other lung epithelial cells, particularly alveolar type II cells.Expression of T1␣ is developmentally regulated (2, 3). Both mRNA and protein are expressed in many fore-and midgut derivatives as early as embryonic day 10.5 (rat) including the primitive lung (day 12.5) and the anterior pituitary anlage (Rathke's pouch), in the early embryonic brain, spinal cord, other neural structures, and several other organs. In most of these tissues, however, expression is rapidly repressed during fetal development (brain) or postnatally (bronchiolar epithelium). In the adult rat, T1␣ mRNA and protein expression can be detected at high levels only in the alveolar type I cell, in choroid plexus epithelium, in ciliary body of the eye, and in a subset of osteoblasts (4, 5). These complex developmental temporal-spatial patterns suggest that active mechanisms of gene regulation determine the highly specific pattern of T1␣ expression in the adult.In situ hybridization, immunocytochemical, biochemical, and molecular analyses (2, 6) show that adult alveolar type II cells do not express T1␣ in vivo, although these cells reside in the alveolar epithelium and act as stem cells to generate new type I cells in normal and injured lung (7). However, when type II cells from normal lung are cultured under conditions where they do not proliferate, they rapidly (within Ͻ24 h) express both T1␣ mRNA and protein, while down-regulating type II cell genes (8).These and other similar findings suggest that type II and type I cell genes share certain common regulatory elements and transactivating molecules but not others, allowing for expression of their cell-specific phenotypes. There is now considerable information about the regulation of type II cell genes because of an interest in defining the molecular control of synthesis of pulmonary surfactant, a complex lipid-protein material secreted by type II cells. The promoters for surfactant protein (SP) 1 -A (9 -12), -B (13-17), -C (18, 19), -D (20), and Clara cell-specific protein (CCSP) (21-24) genes have been partially characterized, and some cis-regulatory elements and transactivating proteins have been identified. Most of these genes have in common their transactivation by 14,

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Synergistic transcriptional activation of the thyrotropin receptor promoter by cyclic AMP-responsive-element-binding protein and thyroid transcription factor 1

Cited by 12 publications

References 34 publications

Thyroid Regulatory Factors

Thyroid Regulatory Factors

Thyrostimulin, but Not Thyroid-stimulating Hormone (TSH), Acts as a Paracrine Regulator to Activate the TSH Receptor in Mammalian Ovary

TGT3, Thyroid Transcription Factor I, and Sp1 Elements Regulate Transcriptional Activity of the 1.3-Kilobase Pair Promoter ofT1α, a Lung Alveolar Type I Cell Gene

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