scholarly journals Retinoic acid receptor beta2 and neurite outgrowth in the adult mouse spinal cord in vitro

2002 ◽  
Vol 115 (19) ◽  
pp. 3779-3786 ◽  
Author(s):  
J. Corcoran
Keyword(s):  
Spinal Cord ◽  
Retinoic Acid ◽  
Neurite Outgrowth ◽  
Adult Mouse ◽  
Retinoic Acid Receptor ◽  
Mouse Spinal Cord ◽  
Acid Receptor

Differential RA responsiveness among subsets of mouse late progenitor spermatogonia

Reproduction ◽  
2021 ◽  
Author(s):  
Shinnosuke Suzuki ◽  
John R. McCarrey ◽  
Brian P Hermann
Keyword(s):  
Stem Cells ◽  
Retinoic Acid ◽  
Single Cell ◽  
Adult Mouse ◽  
Retinoic Acid Receptor ◽  
Mouse Testis ◽  
Rna Seq ◽  
Reporter Expression ◽  
Acid Receptor ◽  
Whole Mount

Initiation of spermatogonial differentiation in the mouse testis begins with the response to retinoic acid (RA) characterized by activation of KIT and STRA8 expression. In the adult, spermatogonial differentiation is spatiotemporally coordinated by a pulse of RA every 8.6 days that is localized to stages VII-VIII of the seminiferous epithelial cycle. Dogmatically, progenitor spermatogonia that express retinoic acid receptor gamma (RARG) at these stages will differentiate in response to RA, but this has yet to be tested functionally. Previous single-cell RNA-seq data identified phenotypically and functionally distinct subsets of spermatogonial stem cells (SSCs) and progenitor spermatogonia, where late progenitor spermatogonia were defined by expression of RARG and Dppa3. Here, we found late progenitor spermatogonia (RARGhigh KIT-) were further divisible into two subpopulations based on Dppa3 reporter expression (Dppa3-ECFP or Dppa3-EGFP) and were observed across all stages of the seminiferous epithelial cycle. However, nearly all Dppa3+ spermatogonia were differentiating (KIT+) late in the seminiferous epithelial cycle (stages X-XII), while Dppa3- late progenitors remained abundant, suggesting that Dppa3+ and Dppa3- late progenitors differentially responded to RA. Following acute RA treatment (2-4hr), significantly more Dppa3+ late progenitors induced KIT, including at the midpoint of the cycle (stages VI-IX), than Dppa3- late progenitors. Subsequently, single-cell analyses indicated a subset of Dppa3+ late progenitors expressed higher levels of Rxra, which we confirmed by RXRA whole-mount immunostaining. Together, these results indicate RARG alone is insufficient to initiate a spermatogonial response to RA in the adult mouse testis and suggest differential RXRA expression may discriminate responding cells.

scholarly journals Inhibitory effect of retinoic acid receptor agonists on in vitro chondrogenic differentiation

2019 ◽  
Vol 95 (2) ◽  
pp. 202-208
Author(s):  
Yusuke Sumitani ◽  
Kenta Uchibe ◽  
Kaya Yoshida ◽  
Yao Weng ◽  
Jiajie Guo ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Chondrogenic Differentiation ◽  
Retinoic Acid Receptor ◽  
Inhibitory Effect ◽  
Acid Receptor ◽  
Receptor Agonists

scholarly journals Effects of Vitamin-A Status on Hamster Tracheal Epithellum in Viva in Vitro

1989 ◽  
Vol 11 (3) ◽  
pp. 1-6 ◽  
Author(s):  
Luigi M. De Luca ◽  
Elizabeth M. McDowell
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Retinoic Acid Receptor ◽  
Normal Liver ◽  
Acid Receptor ◽  
New Horizons ◽  
Vitamin A Status ◽  
Essential Nutrient ◽  
Hepatoma Tissue

In this paper we have suggested the new concept of exotrophic cells, i.e. cells that have conditionally escaped the need for an essential nutrient, such as vitamin A. These exotrophs might become fixed by a mutation and eventually contribute to the tumorigenic phenotype. The discovery of the retinoic acid receptor (RAR) has opened up new horizons in the search for the mechanism of action of retinoic acid [17; 18]. It is intriguing that a second retinoic acid receptor, RARE, is abundantly expressed in hepatoma tissue and not in normal liver; Benbrook et al. [191 suggest that the erroneous expression of the RARE might contribute to tumour development in liver. How and whether these findings relate to the vitamin-A-deficient status of hepatoma cells remains to be understood.

scholarly journals Attenuation of Hypertrophy in Human MSCs via Treatment with a Retinoic Acid Receptor Inverse Agonist

2020 ◽  
Vol 21 (4) ◽  
pp. 1444 ◽  
Author(s):  
Moritz Riedl ◽  
Christina Witzmann ◽  
Matthias Koch ◽  
Siegmund Lang ◽  
Maximilian Kerschbaum ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cell Fate ◽  
Limb Development ◽  
Retinoic Acid Receptor ◽  
Cartilage Regeneration ◽  
Inverse Agonist ◽  
Cartilage Tissue ◽  
Human Mscs ◽  
Acid Receptor

In vitro chondrogenically differentiated mesenchymal stem cells (MSCs) have a tendency to undergo hypertrophy, mirroring the fate of transient “chondrocytes” in the growth plate. As hypertrophy would result in ossification, this fact limits their use in cartilage tissue engineering applications. During limb development, retinoic acid receptor (RAR) signaling exerts an important influence on cell fate of mesenchymal progenitors. While retinoids foster hypertrophy, suppression of RAR signaling seems to be required for chondrogenic differentiation. Therefore, we hypothesized that treatment of chondrogenically differentiating hMSCs with the RAR inverse agonist, BMS204,493 (further named BMS), would attenuate hypertrophy. We induced hypertrophy in chondrogenic precultured MSC pellets by the addition of bone morphogenetic protein 4. Direct activation of the RAR pathway by application of the physiological RAR agonist retinoic acid (RA) further enhanced the hypertrophic phenotype. However, BMS treatment reduced hypertrophic conversion in hMSCs, shown by decreased cell size, number of hypertrophic cells, and collagen type X deposition in histological analyses. BMS effects were dependent on the time point of application and strongest after early treatment during chondrogenic precultivation. The possibility of modifing hypertrophic cartilage via attenuation of RAR signaling by BMS could be helpful in producing stable engineered tissue for cartilage regeneration.

scholarly journals Ligand-Activated Retinoic Acid Receptor Inhibits AP-1 Transactivation by Disrupting c-Jun/c-Fos Dimerization

1999 ◽  
Vol 13 (2) ◽  
pp. 276-285 ◽  
Author(s):  
Xiao-Feng Zhou ◽  
Xi-Qiang Shen ◽  
Lirim Shemshedini
Keyword(s):  
Retinoic Acid ◽  
Dna Binding ◽  
Transcriptional Activity ◽  
Retinoic Acid Receptor ◽  
Cellular Growth ◽  
Dependent Manner ◽  
Acid Receptor ◽  
Retinoid Receptors ◽  
Two Hybrid

Abstract In the presence of retinoic acid (RA), the retinoid receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), are able to up-regulate transcription directly by binding to RA-responsive elements on the promoters of responsive genes. Liganded RARs and RXRs are also capable of down-regulating transcription, but, by contrast, this is an indirect effect, mediated by the interaction of these nuclear receptors not with DNA but the transcription factor activating protein-1 (AP-1). AP-1 is a dimeric complex of the protooncoproteins c-Jun and c-Fos and directly regulates transcription of genes important for cellular growth. Previous in vitro results have suggested that RARs can block AP-1 DNA binding. Using a mammalian two-hybrid system, we report here that human RARα (hRARα) can disrupt in a RA-dependent manner the homo- and heterodimerization properties of c-Jun and c-Fos. This inhibition of dimerization is cell specific, occurring only in those cells that exhibit RA-induced repression of AP-1 transcriptional activity. Furthermore, this mechanism appears to be specific for the RARs, since another potent inhibitor of AP-1 activity, the glucocorticoid receptor, does not affect AP-1 dimerization. Our data argue for a novel mechanism by which RARs can repress AP-1 DNA binding, in which liganded RARs are able to interfere with c-Jun/c-Jun homodimerization and c-Jun/c-Fos heterodimerization and, in this way, may prevent the formation of AP-1 complexes capable of DNA binding.

scholarly journals Pharmacological Activity of Retinoic Acid Receptor Alpha-Selective Antagonists in Vitro and in Vivo

2013 ◽  
Vol 4 (5) ◽  
pp. 446-450 ◽  
Author(s):  
Sanny S. W. Chung ◽  
Rebecca A. D. Cuellar ◽  
Xiangyuan Wang ◽  
Peter R. Reczek ◽  
Gunda I. Georg ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Pharmacological Activity ◽  
Retinoic Acid Receptor ◽  
Retinoic Acid Receptor Alpha ◽  
Acid Receptor ◽  
Receptor Alpha ◽  
Selective Antagonists
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