scholarly journals Effect of retinoid status on α, β and γ retinoic acid receptor mRNA levels in various rat tissues

1992 ◽  
Vol 286 (3) ◽  
pp. 755-760 ◽  
Author(s):  
S Kato ◽  
H Mano ◽  
T Kumazawa ◽  
Y Yoshizawa ◽  
R Kojima ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Vitamin A ◽  
Retinoic Acid Receptor ◽  
Rat Tissues ◽  
Mrna Levels ◽  
Acid Receptor ◽  
Beta Gene

We have investigated the effects of retinoids, vitamin D and thyroid hormone on the levels of retinoic acid receptor (RAR)alpha, RAR beta and RAR gamma mRNAs in intact animals. Although vitamin A deficiency caused no significant changes in the levels of RAR alpha and RAR gamma mRNAs, the level of RAR beta transcripts was greatly decreased in various tissues of vitamin A-deficient rats, but was restored rapidly to a normal level after administration of retinoic acid. Retinol also restored the RAR beta mRNA level, but the magnitude and kinetics of the induction differed from those by retinoic acid. The use of specific inhibitors demonstrated that this autoregulation of RAR beta gene expression in vivo occurred at the transcriptional level. In addition, from these results it was postulated that the maintenance of the normal RAR beta mRNA levels seemed to require a threshold serum retinol concentration (about 25 micrograms/dl). Moreover, we found that administration of retinol and retinoic acid to normal rats caused the overexpression of RAR beta transcripts (2-15-fold) when compared with the control levels of RAR beta mRNA, although the levels of RAR alpha and RAR gamma mRNAs were not affected. Vitamin D and thyroid hormone did not modulate the levels of RAR transcripts. These findings clearly indicate the specific ligand regulation of RAR beta gene expression in intact animals. The altered levels of RAR beta according to retinoid status may affect retinoid-inducible gene expression.

Detection of retinoic acid receptor mRNA in rat tissues by reverse transcriptase-polymerase chain reaction

1992 ◽  
Vol 9 (3) ◽  
pp. 291-294 ◽  
Author(s):  
Y.-J. Y. Wan ◽  
L. Wang ◽  
T.-C. J. Wu
Keyword(s):  
Polymerase Chain Reaction ◽  
Retinoic Acid ◽  
Reverse Transcriptase ◽  
Retinoic Acid Receptor ◽  
Rat Tissues ◽  
Mrna Levels ◽  
Chain Reaction ◽  
Dominant Form ◽  
Acid Receptor ◽  
Polymerase Chain

ABSTRACT The presence of retinoic acid receptor (RAR) α, β and γ mRNA was examined in 16 different kinds of rat tissue using the highly sensitive reverse transcriptase-polymerase chain reaction technique. The data demonstrated that each tissue expressed at least two types of RAR mRNA. Among the three types of RAR mRNA, RAR α was widely expressed in all types of organ and was the dominant form expressed in the gastrointestinal tract. RAR β mRNA was not present in the intestine and spleen. In addition, RAR β mRNA levels were high in the heart, lung, brain, testis and epididymis. RAR γ mRNA was abundant in both male and female reproductive systems, as well as epidermal tissues. The prevalence of each RAR mRNA in the tissues suggests the diverse biological roles of these receptors.

scholarly journals Alteration of Cerebellar Neurotropin Messenger Ribonucleic Acids and the Lack of Thyroid Hormone Receptor Augmentation by staggerer-Type Retinoic Acid Receptor-Related Orphan Receptor-α Mutation

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1745-1753 ◽  
Author(s):  
Chun-Hong Qiu ◽  
Noriaki Shimokawa ◽  
Toshiharu Iwasaki ◽  
Ishwar S. Parhar ◽  
Noriyuki Koibuchi
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Retinoic Acid Receptor ◽  
Orphan Receptor ◽  
Granule Cell Layer ◽  
Mrna Levels ◽  
Response Element ◽  
Altered Expression ◽  
Acid Receptor

The mutant mouse staggerer (sg) harbors a deletion within the gene encoding the retinoic acid receptor-related orphan receptor-α (RORα). Homozygotes show aberrant cerebellar development. However, the mechanisms responsible for the cerebellar defect are still poorly understood. In the present study, the involvement of neurotropins (NTs), including nerve growth factor, brain-derived neurotropic factor, NT-3 and NT-4/5, and their receptors, which play a crucial role in brain development, on the cerebellar defects of sg mice was studied by semiquantitative RT-PCR and in situ hybridization histochemistry. An evident alteration of these mRNA levels was observed in both heterozygotes and homozygotes. Such difference was most evident in the internal granule cell layer. Because the changes in NT expression as well as morphological alterations in sg cerebellum are similar to those in hypothyroid animals, the effect of mutant RORα (RORsg) on transcriptional regulation through the thyroid hormone (TH) response element or the ROR response element (RORE) was then studied. RORsg neither activated the transcription through RORE nor suppressed RORα-induced transcription, indicating that it does not function as a dominant negative inhibitor. On the other hand, although wild-type RORα augmented TH receptor (TR)α1/β1-mediated transcription through various TH response elements, RORsg was not effective in augmenting TR action. These results suggest that the cerebellar defect of the sg mouse is partly caused by the altered expression of NTs and the lack of augmentation of TR-mediated transcription by RORα as well as the absence of RORα action through RORE.

scholarly journals Induction of nephrin gene expression by selective cooperation of the retinoic acid receptor and the vitamin D receptor

2009 ◽  
Vol 24 (10) ◽  
pp. 3006-3012 ◽  
Author(s):  
Maro Okamura ◽  
Yosuke Takano ◽  
Yukinori Saito ◽  
Jian Yao ◽  
Masanori Kitamura
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Retinoic Acid ◽  
Vitamin D Receptor ◽  
Retinoic Acid Receptor ◽  
Acid Receptor

Retinoic Acid Receptor-α Gene Expression Is Modulated by Dietary Vitamin A and by Retinoic Acid in Chicken T Lymphocytes

1994 ◽  
Vol 124 (11) ◽  
pp. 2139-2146 ◽  
Author(s):  
Orna Halevy ◽  
Yossef Arazi ◽  
Doron Melamed ◽  
Aharon Friedman ◽  
David Sklan
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
T Lymphocytes ◽  
Vitamin A ◽  
Retinoic Acid Receptor ◽  
Dietary Vitamin ◽  
Acid Receptor ◽  
Retinoic Acid Receptor Α

scholarly journals The Environmental Light Influences the Circulatory Levels of Retinoic Acid and Associates with Hepatic Lipid Metabolism

Endocrinology ◽  
2008 ◽  
Vol 149 (12) ◽  
pp. 6336-6342 ◽  
Author(s):  
Wenqiang Pang ◽  
Chunying Li ◽  
Yue Zhao ◽  
Shiming Wang ◽  
Wei Dong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Adenosine Receptors ◽  
Light Exposure ◽  
Retinoic Acid Receptor ◽  
Hepatic Lipase ◽  
Mouse Retina ◽  
Acid Receptor ◽  
Hepatic Lipid ◽  
Environmental Light

Environmental light is involved in the regulation of photochemical reaction in mouse retina. It remains unclear whether light-mediated increase in all-trans retinoic acid (ATRA) synthesis in retina will result in altering the circulatory levels of ATRA and regulating downstream gene expression and physiological function. Here we showed circulatory levels of ATRA decreased in mice under constant darkness and elevated by light exposure. Fat gene pancreatic lipase-related protein 2 (mPlrp2) and its partner procolipase (mClps), but not hepatic lipase (mHl), activated in livers for responding to lack of light illuminating. Light-triggered alterations in circulatory ATRA levels regulated ecto-5′-nucleotidase gene expression by retinoic acid receptor retinoic acid receptor-α and modulated 5′-AMP levels in blood and were associated with mPlrp2 and mClps expression in the livers. Mice deficient in adenosine receptors displayed mPlrp2 and mClps expression in livers under 12-h light, 12-h dark cycles. Caffeine blocked adenosine receptors and induced hepatic mPlrp2 and mClps expression in wild-type mice. Mice activated in hepatic mPlrp2 and mClps expression lowered hepatic and serum lipid levels and markedly elevated circulatory levels of all-trans retinol. Our results suggest environmental light influence hepatic lipid homeostasis by light-modulated retinoic acid signaling associated with mPlrp2 and mClps gene expression in livers.

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