Regulation of thyroid hormone receptor β-2 mRNA levels by retinoic acid

Jones, Kenneth M.; Yaffe, Barry M.; Chin, William W.

doi:10.1016/0303-7207(93)90262-i

Cited by 16 publications

(6 citation statements)

References 29 publications

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“…3 In consistence with this observation, the current study demonstrated that RA induced nuclear factors binding to this HRE and inhibited the activities of reporters carrying this HRE in P19. In other studies, the T 3 R ␤ gene was shown to be induced by RA (31). In this study, it was clearly demonstrated that T 3 R ␤1 was able to bind to this HRE and that its expression suppressed the CRABP-lacZ reporter activities.…”

Section: Discussionsupporting

confidence: 60%

“…Biological Activities and DR4 Binding of T 3 R ␤1 , RARs, and RXR ␤ -Because many genes could be induced by RA in embryonic stem cells (30) and P19 cells, 2 such as several RARs/RXRs, thyroid hormone receptors (31), and some homeobox genes, we then tested the effects of three RARs, RXR ␤ , and T 3 R ␤1 on the wild-type reporter and DR4 mutants in co-transfection experiments as shown in Fig. 7A.…”

Section: Ra Induction Of Nuclear Factors Binding To the Negative Hre mentioning

confidence: 99%

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Characterization of a Negative Response DNA Element in the Upstream Region of the Cellular Retinoic Acid-binding Protein-I Gene of the Mouse

Wei

1997

Journal of Biological Chemistry

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A negative, regulatory DNA element from the mouse cellular retinoic acid-binding protein I gene promoter was identified. This DNA element, located approximately 1 kilobase upstream from the transcription initiation site of this gene, contained a pair of direct repeats (DRs) separated by 4 base pairs (DR4, TGAC-CTTTGGGGACCT). By examining a series of reporters deleted or mutated within this DR4 region, it was concluded that the core sequence of this DR4, including both repeats and the spacer, was required for suppressive activity in the mouse embryonal carcinoma cell line P19. From gel retardation experiments, it was concluded that both repeated sequences were essential for specific protein binding, but the spacer sequence was not as critical. Specific residues required for protein binding to this DR4 were identified. In P19 cells, retinoic acid induced the binding of nuclear factors to DR4 and suppressed the activities of the reporters containing this DR4. Co-expression of retinoic acid receptor ␤ or thyroid hormone receptor ␤1 (T 3 R ␤1 ) significantly inhibited the expression of this reporter in P19 cells. Gel retardation with in vitro-synthesized nuclear receptors demonstrated specific binding of this DR4 by T 3 R ␤1 monomers, homodimers, or heterodimers of T 3 R ␤1 / retinoid receptor X ␤. A biological function of DR4 in crabp-I gene regulation in P19 cells was suggested.

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Section: Discussionsupporting

confidence: 60%

Section: Ra Induction Of Nuclear Factors Binding To the Negative Hre mentioning

confidence: 99%

Characterization of a Negative Response DNA Element in the Upstream Region of the Cellular Retinoic Acid-binding Protein-I Gene of the Mouse

Wei

1997

Journal of Biological Chemistry

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“…Though the murine TR 2 promoter has recently been cloned, the regulation of TR 2 gene expression remains unclear (Wood et al 1994). There are data to suggest that TR 2 expression is also regulated at both transcriptional and post-transcriptional levels (Jones et al 1993). It is thus possible that the selective thyromimetic effects of T 2 , at least partially, reflect post-transcriptional events.…”

Section: Discussionmentioning

confidence: 99%

3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitro

Ball¹,

Sokolov²,

Ww³

1997

Journal of Molecular Endocrinology

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Recent data have suggested that the iodothyronine, 3,5-diiodo-l-thyronine (T 2 ), has selective thyromimetic activity. In vivo, T 2 has been shown to suppress TSH levels at doses that do not produce significant peripheral manifestations of thyroid hormone activity. Furthermore, T 2 has been shown to produce smaller increments in peripheral indices of thyroid status than does T 3 , when doses resulting in equivalent suppression of circulating TSH are compared. We have assessed the selective thyromimetic activity of T 2 in vivo and in vitro, and performed in vitro studies to assess the potential molecular basis for these selective properties. T 2 was 100-fold less potent than T 3 in stimulating GH mRNA levels in GH 3 cells. In contrast, the iodothyronines were almost equivalent in their ability to downregulate TR 2 mRNA levels in this cell line. Both 3,3 -diiodo--thyronine and thyronine exhibited no significant thyromimetic effects on either process. In vivo, doses of T 2 and T 3 that were equivalent in their induction of hepatic malic enzyme (ME) mRNA did not produce equivalent suppression of circulating TSH, with T 2 being only 27% as effective as T 3 . T 2 was up to 500-fold less potent than T 3 in displacing [125 I]-T 3 from in vitro translated specific nuclear receptors (TRs) and GH 3 cell nuclear extracts. Electrophoretic mobility shift assays, assessing the ability of T 2 to produce dissociation of TR 1 homodimers from inverted palindrome T 3 response elements, indicated that T 2 was also 1000-fold less potent than T 3 in this respect. These data confirm that T 2 has significant thyromimetic activity, and that this activity is selective both in vivo and in vitro. However, there are no data to support a selective central effect, T 2 being relatively more potent in stimulating hepatic ME mRNA than in suppression of TSH in vivo. The basis for this differential thyromimetic activity is not selective affinity of the different TR isoforms for T 2 , or divergent properties of T 2 in competitive binding and functional assays in vitro.

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“…In this study we examined the expression of known coactivator [steroid receptor coactivator-1 (SRC-1) (10) and E1A-associated 300-kDa protein (p300) (11)] and corepressor [SMRT) (3) and (N-CoR) (2)] genes in a large number of tissues, including several endocrine glands and cell lines, to provide a comparative analysis of their mRNA expression patterns. The mRNAs encoding several members of the steroid/ thyroid hormone receptor superfamily [TRs, retinoic acid receptors (RARs), and retinoid X receptors (RXRs)] have been shown either to increase or decrease in response to treatment with their cognate hormones (12)(13)(14) or with heterologous hormones [i.e. effect of estradiol (E 2 ) on different TR and RXR isoforms (Schomburg, L., manuscript in preparation)].…”

mentioning

confidence: 99%

Expression and Hormonal Regulation of Coactivator and Corepressor Genes

et al. 1998

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Steroid/thyroid/retinoid receptors are members of the nuclear receptor superfamily and ligand-inducible transcription factors. These receptors modulate transcription of various cellular genes, either positively or negatively, by interacting with specific hormone-response elements located in the target gene promoters. Recent data show that nuclear receptors enhance or inhibit transcription by recruiting an array of coactivator and corepressor proteins to the transcription complex. We examined and compared the expression of four coactivator (steroid receptor coactivator-1 and E1A-associated 300-kDa protein) and corepressor (SMRT and N-CoR) genes in a number of tissues including several endocrine glands and cell lines. We also addressed whether their messenger RNA levels are hormonally regulated by studying the effects of thyroid hormone (T3) and estrogen (E2) treatment in rat pituitary cells (GH3) in vitro and in anterior pituitary in vivo. Our studies show that there are distinct tissue-specific expression patterns of these genes. We show that T3 and E2 regulate the expression of steroid receptor coactivator-1 messenger RNA in the anterior pituitary in addition to a gender-related difference. These tissue variations may have physiological implications for heterogeneity of hormone responses that are observed in normal and malignant tissues.

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Regulation of thyroid hormone receptor β-2 mRNA levels by retinoic acid

Cited by 16 publications

References 29 publications

Characterization of a Negative Response DNA Element in the Upstream Region of the Cellular Retinoic Acid-binding Protein-I Gene of the Mouse

Characterization of a Negative Response DNA Element in the Upstream Region of the Cellular Retinoic Acid-binding Protein-I Gene of the Mouse

3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitro

Expression and Hormonal Regulation of Coactivator and Corepressor Genes

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