Retinoic acid and dexamethasone interact to regulate S14 gene transcription in 3T3-F442A adipocytes

Lepar, Gerald J.; Jump, Donald Β.

doi:10.1016/0303-7207(92)90072-e

Cited by 20 publications

(17 citation statements)

References 46 publications

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“…Figure 2A shows that 3T3-L1 preadipocytes were found to express primarily RAR␣ and RAR␥, in agreement with the results of earlier reports (29,46,58). RAR␣ mRNA levels were essentially unchanged during the course of adipocyte differentiation.…”

Section: Ra Inhibition Of Adipocyte Differentiation Is Mediated Bysupporting

confidence: 91%

Distinct Stages in Adipogenesis Revealed by Retinoid Inhibition of Differentiation after Induction of PPARγ

Xue

Schwarz

Chawla

et al. 1996

Molecular and Cellular Biology

173

164

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Retinoic acid (RA) inhibits adipocyte differentiation of 3T3-L1 preadipocytes but is effective only early in adipogenesis. RA prevented induction of the adipogenic factors PPAR␥ and C/EBP␣. Using receptor-specific ligands, we determined that the effects of RA were mediated by liganded RA receptors (RARs) rather than retinoid X receptors. Preadipocytes expressed primarily RAR␣ and RAR␥; during adipocyte differentiation, RAR␣ gene expression was nearly constant, whereas RAR␥1 mRNA and protein levels dramatically decreased. Ectopic expression of RAR␥1 extended the period of effectiveness of RA by 24 to 48 h; RAR␣ expression had a similar effect, suggesting functional redundancy of RAR subtypes. Remarkably, RA inhibited differentiation when added after PPAR␥1 and PPAR␥2 proteins had already been expressed and resulted in the loss of PPAR␥ proteins from cells. By 72 to 96 h after the induction of differentiation, RA failed to prevent differentiation of even ectopic-RAR-expressing cells. Thus, the unresponsiveness of 3T3-L1 preadipocytes to RA after the induction of differentiation is initially due to the reduction in cellular RAR concentration rather than to the induction of PPAR␥. At later times cells continue along the differentiation pathway in a manner which is RA and RAR independent.

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Section: Ra Inhibition Of Adipocyte Differentiation Is Mediated Bysupporting

confidence: 91%

Distinct Stages in Adipogenesis Revealed by Retinoid Inhibition of Differentiation after Induction of PPARγ

Xue

Schwarz

Chawla

et al. 1996

Molecular and Cellular Biology

173

164

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“…In previous studies, nuclear retinoic acid receptor (RAR) a and g upregulation has been found in ATRA-treated adipocytes [37,38]. In our study, we also determined the effect of ATRA on RARa and g expression.…”

Section: Activation Of Rarg Is Responsible For Atra-exhibited Inhibitmentioning

confidence: 88%

RARγ-C-Fos-PPARγ2 signaling rather than ROS generation is critical for all-trans retinoic acid-inhibited adipocyte differentiation

et al. 2014

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“…Moreover, differentiated adipocytes respond to RA with a rapid increase in S14 (40) and phosphoenolpyruvate carboxykinase gene transcription (41). A goal of the present work was a functional analysis in transfected cells of cis-acting elements present in rat ucp enhancer and involved in RA activation of ucp gene transcription.…”

Section: Dna Mobility Shift Binding Activity Of Ir2 Reveals Binding Omentioning

confidence: 99%

Essential cis-Acting Elements in Rat Uncoupling Protein Gene Are in an Enhancer Containing a Complex Retinoic Acid Response Domain

Larose¹,

Cassard-Doulcier²,

Fleury³

et al. 1996

Journal of Biological Chemistry

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Transgenic mice were generated with a transgene containing the 211-base pair (bp) enhancer and 0.4 kilobase pairs of 5-flanking DNA of the uncoupling protein (ucp) gene. Expression of this transgene was restricted to brown adipose tissue and was inducible by cold exposure or treatment of transgenic mice by norepinephrine, retinoic acid (RA), or CL-316,243 ␤3-adrenoreceptor agonist. A search for retinoic acid response elements in the ucp gene enhancer was undertaken using mutagenesis and transfection of cultured cells with chloramphenicol acetyltransferase constructs. Deletion or mutations of several putative retinoic acid response elements were ineffective. Mutations of a TGAATCA region dramatically decreased the transcriptional activity in the presence of RA. In vitro this region was able to bind a complex containing proteins recognized by antibodies against Jun or Fos. Mutations of an adjacent region related to an inverted repeat of type 2 also markedly decreased RA effect. This region was able to bind in vitro retinoid X receptor ␣ and retinoic acid receptor ␤. The two regions form an activating region between bp ؊2421 and ؊2402 (referred to as the ucp gene-activating region), which has an enhancer activity but cannot confer RA response to a promoter. This response was obtained with a larger DNA fragment (bp ؊2489 to ؊2398) constituting a complex RA response domain.

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Retinoic acid and dexamethasone interact to regulate S14 gene transcription in 3T3-F442A adipocytes

Cited by 20 publications

References 46 publications

Distinct Stages in Adipogenesis Revealed by Retinoid Inhibition of Differentiation after Induction of PPARγ

Distinct Stages in Adipogenesis Revealed by Retinoid Inhibition of Differentiation after Induction of PPARγ

RARγ-C-Fos-PPARγ2 signaling rather than ROS generation is critical for all-trans retinoic acid-inhibited adipocyte differentiation

Essential cis-Acting Elements in Rat Uncoupling Protein Gene Are in an Enhancer Containing a Complex Retinoic Acid Response Domain

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