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Academic literature on the topic 'Deficiency; Retinoid pathway gene expression'
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Journal articles on the topic "Deficiency; Retinoid pathway gene expression"
1
Baleato, R. M., R. J. Aitken, and S. D. Roman. "244.Interaction between bone morphogenetic protein 4 and retinoid signalling in mouse spermatogenesis." Reproduction, Fertility and Development 16, no. 9 (2004): 244. http://dx.doi.org/10.1071/srb04abs244.
Full textAbstract:
Vitamin A (retinol, or ROL) is also essential for normal spermatogenesis in the rat and mouse. Vitamin A-deficient (VAD) rodents suffer various disorders including blindness and male infertility. The molecular mechanisms leading to infertility in vitamin A deficient rodents have never been fully elucidated. Following prolonged vitamin A withdrawal the only germ cells remaining in the VAD rodent testis are stem cell spermatogonia, type A1 spermatogonia, and a few preleptotene spermatocytes. Supplementing the diet of these animals with retinoic acid (RA) alleviates all symptoms of vitamin A deficiency, with the exception of sight and spermatogenesis. It is not until VAD animals are re-administered ROL through the diet, or RA is injected in repeated high doses directly into the testis, that normal spermatogenic function is restored. Here we report an interaction, in germ cells, between the Bone Morphogenetic Protein (BMP) 4 and retinoid signalling pathways that may help explain the molecular mechanics of vitamin A deficiency. We localised BMP4 gene expression to adult germ cells, in particular spermatogonia, at both the mRNA and protein level. We generated VAD mice and found that in the absence of retinoids in vivo, bmp4 gene expression was significantly upregulated in the testis. We also observed that the expression of bmp4 is downregulated by retinoid treatment in germ cells isolated from vitamin A sufficient mice. Expression of bmp4 mRNA in isolated spermatogonia was more sensitive to ROL rather than RA. Our results may reflect a direct requirement for ROL by germ cells for the resumption of spermatogenesis in VAD animals that involves the regulation of BMP4 expression. Furthermore our observations suggest that retinoid signalling in germ cells is different to that observed in somatic cells, and may provide insights into the role of retinoids in spermatogenesis.
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Ruberte, E., V. Friederich, P. Chambon, and G. Morriss-Kay. "Retinoic acid receptors and cellular retinoid binding proteins. III. Their differential transcript distribution during mouse nervous system development." Development 118, no. 1 (May 1, 1993): 267–82. http://dx.doi.org/10.1242/dev.118.1.267.
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We have studied the transcript distribution of the retinoic acid receptors (RARs) and the cytoplasmic retinoid binding proteins during embryonic development of the mouse nervous system. Of the three retinoic acid receptors, only RAR-gamma was not expressed in developing neural structures. RAR-beta and RAR-alpha both showed rostral limits of expression in the medulla oblongata equivalent to their patterns of expression in the neuroepithelium of the early hindbrain neural tube. Within their expression domains in the spinal cord and brain, RAR-alpha was ubiquitously expressed, whereas RAR-beta transcripts showed very specific patterns of expression, suggesting that this receptor is involved in mediating retinoic acid-induced gene expression in relation to the development of specific neural structures or pathways. The cytoplasmic binding proteins, cellular retinoic acid binding proteins type I and II (CRABP I and CRABP II) and cellular retinol binding protein type I (CRBP I), were widely distributed in developing neural structures. Their differential spatiotemporal patterns of expression suggest that fine regional control of availability of retinoic acid (RA) to the nuclear receptors plays an important role in organization and differentiation of the nervous system. For instance, expression of CRABP I in the migrating cells that give rise to the olivary and pontine nuclei, which develop abnormally in conditions of retinoid excess, is consistent with observations from a variety of other systems indicating that CRABP I limits the access of RA to the nuclear receptors in normal physiological conditions. Similarly, expression of CRBP I in the choroid plexuses, which develop abnormally in conditions of vitamin A deficiency, is consistent with observations indicating that this binding protein mediates the synthesis of RA in tissues requiring high levels of RA for their normal developmental programme. RAR-beta and CRABP II, which are both RA-inducible, were coexpressed with CRBP I in the choroid plexus and in many other sites, perhaps reflecting the fact that all three genes are RA-inducible. The function of CRABP II is not well understood; its domains of expression showed overlaps with both CRABP I and CRBP I.
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Leszczyński, Paweł, Magdalena Śmiech, Aamir Salam Teeli, Effi Haque, Robert Viger, Hidesato Ogawa, Mariusz Pierzchała, and Hiroaki Taniguchi. "Deletion of the Prdm3 Gene Causes a Neuronal Differentiation Deficiency in P19 Cells." International Journal of Molecular Sciences 21, no. 19 (September 29, 2020): 7192. http://dx.doi.org/10.3390/ijms21197192.
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PRDM (PRDI-BF1 (positive regulatory domain I-binding factor 1) and RIZ1 (retinoblastoma protein-interacting zinc finger gene 1) homologous domain-containing) transcription factors are a group of proteins that have a significant impact on organ development. In our study, we assessed the role of Prdm3 in neurogenesis and the mechanisms regulating its expression. We found that Prdm3 mRNA expression was induced during neurogenesis and that Prdm3 gene knockout caused premature neuronal differentiation of the P19 cells and enhanced the growth of non-neuronal cells. Interestingly, we found that Gata6 expression was also significantly upregulated during neurogenesis. We further studied the regulatory mechanism of Prdm3 expression. To determine the role of GATA6 in the regulation of Prdm3 mRNA expression, we used a luciferase-based reporter assay and found that Gata6 overexpression significantly increased the activity of the Prdm3 promoter. Finally, the combination of retinoic acid receptors α and β, along with Gata6 overexpression, further increased the activity of the luciferase reporter. Taken together, our results suggest that in the P19 cells, PRDM3 contributed to neurogenesis and its expression was stimulated by the synergism between GATA6 and the retinoic acid signaling pathway.
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Hu, Qi-Xin, Hui-Yi Wang, Lu Jiang, Chen-Yu Wang, Lin-Gao Ju, Yuan Zhu, Bo Zhong, Min Wu, Zhen Wang, and Lian-Yun Li. "Histone demethylase LSD1 promotes RIG-I poly-ubiquitination and anti-viral gene expression." PLOS Pathogens 17, no. 9 (September 16, 2021): e1009918. http://dx.doi.org/10.1371/journal.ppat.1009918.
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Under RNA virus infection, retinoic acid-inducible gene I (RIG-I) in host cells recognizes viral RNA and activates the expression of type I IFN. To investigate the roles of protein methyltransferases and demethylases in RIG-I antiviral signaling pathway, we screened all the known related enzymes with a siRNA library and identified LSD1 as a positive regulator for RIG-I signaling. Exogenous expression of LSD1 enhances RIG-I signaling activated by virus stimulation, whereas its deficiency restricts it. LSD1 interacts with RIG-I, promotes its K63-linked polyubiquitination and interaction with VISA/MAVS. Interestingly, LSD1 exerts its function in antiviral response not dependent on its demethylase activity but through enhancing the interaction between RIG-I with E3 ligases, especially TRIM25. Furthermore, we provide in vivo evidence that LSD1 increases antiviral gene expression and inhibits viral replication. Taken together, our findings demonstrate that LSD1 is a positive regulator of signaling pathway triggered by RNA-virus through mediating RIG-I polyubiquitination.
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Husson, Marianne, Valérie Enderlin, Serge Alfos, Catherine Féart, Paul Higueret, and Véronique Pallet. "Triiodothyronine administration reverses vitamin A deficiency-related hypo-expression of retinoic acid and triiodothyronine nuclear receptors and of neurogranin in rat brain." British Journal of Nutrition 90, no. 1 (July 2003): 191–98. http://dx.doi.org/10.1079/bjn2003877.
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Recent studies have revealed that retinoids play an important role in the adult central nervous system and cognitive functions. Previous investigations in mice have shown that vitamin A deficiency (VAD) generates a hypo-expression of retinoic acid (RA, the active metabolite of vitamin A) receptors and of neurogranin (RC3, a neuronal protein involved in synaptic plasticity) and a concomitant selective behavioural impairment. Knowing that RC3 is both a triiodothyronine (T3) and a RA target gene, and in consideration of the relationships between the signalling pathways of retinoids and thyroid hormones, the involvement of T3 on RA signalling functionality in VAD was investigated. Thus, the effects of vitamin A depletion and subsequent administration with RA and/or T3 on the expression of RA nuclear receptors (RAR, RXR), T3 nuclear receptor (TR) and on RC3 in the brain were examined. Rats fed a vitamin A-deficient diet for 10 weeks exhibited a decreased expression of RAR, RXR and TR mRNA and of RC3 mRNA and proteins. RA administration to these vitamin A-deficient rats reversed only the RA hypo-signalling in the brain. Interestingly, T3 is able to restore its own brain signalling simultaneously with that of vitamin A and the hypo-expression of RC3. These results obtained in vivo revealed that one of the consequences of VAD is a dysfunction in the thyroid signalling pathway in the brain. This seems of crucial importance since the down regulation of RC3 observed in the depleted rats was corrected only by T3.
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Chen, W. H., G. M. Morriss-Kay, and A. J. Copp. "Genesis and prevention of spinal neural tube defects in the curly tail mutant mouse: involvement of retinoic acid and its nuclear receptors RAR-beta and RAR-gamma." Development 121, no. 3 (March 1, 1995): 681–91. http://dx.doi.org/10.1242/dev.121.3.681.
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A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Using in situ hybridisation and computerised image analysis we show here that in ct/ct embryos, RAR-beta transcripts are deficient in the hindgut endoderm, a tissue whose proliferation rate is abnormal in the ct mutant, and RAR-gamma transcripts are deficient in the tail bud and posterior neuropore region. The degree of deficiency of RAR-gamma transcripts is correlated with the severity of delay of posterior neuropore closure. As early as 2 hours following RA treatment at 10 days 8 hours post coitum, i.e. well before any morphogenetic effects are detectable, RAR-beta expression is specifically upregulated in the hindgut endoderm, and the abnormal expression pattern of RAR-gamma is also altered. These results suggest that the spinal neural tube defects which characterise the curly tail phenotype may be due to interaction between the ct gene product and one or more aspects of the retinoic acid signalling pathway.
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Deis, Jessica A., Hong Guo, Yingjie Wu, Chengyu Liu, David A. Bernlohr, and Xiaoli Chen. "Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes." Journal of Molecular Endocrinology 61, no. 3 (October 2018): 115–26. http://dx.doi.org/10.1530/jme-18-0017.
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Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. The objective of this study was to explore the role and mechanism for LCN2 in the recruitment and retinoic acid-induced activation of brown-like or ‘beige’ adipocytes. We found LCN2 deficiency reduces key markers of thermogenesis including uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) in inguinal white adipose tissue (iWAT) and inguinal adipocytes derived from Lcn2 −/− mice. Lcn2 −/− inguinal adipocytes have attenuated insulin-induced upregulation of thermogenic gene expression and p38 mitogen-activated protein kinase (p38MAPK) signaling pathway activation. This is accompanied by a lower basal and maximal oxidative capacity in Lcn2 −/− inguinal adipocytes, indicating mitochondrial dysfunction. Recombinant Lcn2 was able to restore insulin-induced p38MAPK phosphorylation in both WT and Lcn2 −/− inguinal adipocytes. Rosiglitazone treatment during differentiation of Lcn2 −/− adipocytes is able to recruit beige adipocytes at a normal level, however, further activation of beige adipocytes by insulin and RA is impaired in the absence of LCN2. Further, the synergistic effect of insulin and RA on UCP1 and PGC-1α expression is markedly reduced in Lcn2 −/− inguinal adipocytes. Most intriguingly, LCN2 and the retinoic acid receptor-alpha (RAR-α) are concurrently translocated to the plasma membrane of adipocytes in response to insulin, and this insulin-induced RAR-α translocation is absent in adipocytes deficient in LCN2. Our data suggest a novel LCN2-mediated pathway by which RA and insulin synergistically regulates activation of beige adipocytes via a non-genomic pathway of RA action.
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Tamblyn, J. A., L. E. Jeffery, R. Susarla, D. M. Lissauer, S. L. Coort, A. Muñoz Garcia, K. Knoblich, et al. "Transcriptomic analysis of vitamin D responses in uterine and peripheral NK cells." Reproduction 158, no. 2 (August 2019): 213–23. http://dx.doi.org/10.1530/rep-18-0509.
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Vitamin D deficiency is prevalent in pregnant women and is associated with adverse pregnancy outcomes, in particular disorders of malplacentation. The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), is a potent regulator of innate and adaptive immunity, but its immune effects during pregnancy remain poorly understood. During early gestation, the predominant immune cells in maternal decidua are uterine natural killer cells (uNK), but the responsivity of these cells to 1,25(OH)2D3 is unknown despite high levels of 1,25(OH)2D3 in decidua. Transcriptomic responses to 1,25(OH)2D3 were characterised in paired donor uNK and peripheral natural killer cells (pNK) following cytokine (CK) stimulation. RNA-seq analyses indicated 911 genes were differentially expressed in CK-stimulated uNK versus CK-stimulated pNK in the absence of 1,25(OH)2D3, with predominant differentially expressed pathways being associated with glycolysis and transforming growth factor β (TGFβ). RNA-seq also showed that the vitamin D receptor (VDR) and its heterodimer partner retinoid X receptor were differentially expressed in CK-stimulated uNK vs CK-stimulated pNK. Further analyses confirmed increased expression of VDR mRNA and protein, as well as VDR-RXR target in CK-stimulated uNK. RNA-seq analysis showed that in CK-stimulated pNK, 1,25(OH)2D3 induced 38 and suppressed 33 transcripts, whilst in CK-stimulated uNK 1,25(OH)2D3 induced 46 and suppressed 19 genes. However, multiple comparison analysis of transcriptomic data indicated that 1,25(OH)2D3 had no significant overall effect on gene expression in either CK-stimulated pNK or uNK. These data indicate that CK-stimulated uNK are transcriptionally distinct from pNK and, despite expressing abundant VDR, neither pNK nor uNK are sensitive targets for vitamin D.
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Lefebvre, Bruno, Céline Brand, Sébastien Flajollet, and Philippe Lefebvre. "Down-Regulation of the Tumor Suppressor Gene Retinoic Acid Receptor β2 through the Phosphoinositide 3-Kinase/Akt Signaling Pathway." Molecular Endocrinology 20, no. 9 (September 1, 2006): 2109–21. http://dx.doi.org/10.1210/me.2005-0321.
Full textAbstract:
Abstract The retinoic acid receptor β2 (RARβ2) is a potent, retinoid-inducible tumor suppressor gene, which is a critical molecular relay for retinoid actions in cells. Its down-regulation, or loss of expression, leads to resistance of cancer cells to retinoid treatment. Up to now, no primary mechanism underlying the repression of the RARβ2 gene expression, hence affecting cellular retinoid sensitivity, has been identified. Here, we demonstrate that the phosphoinositide 3-kinase/Akt signaling pathway affects cellular retinoid sensitivity, by regulating corepressor recruitment to the RARβ2 promoter. Through direct phosphorylation of the corepressor silencing mediator for retinoic and thyroid hormone receptors (SMRT), Akt stabilized RAR/SMRT interaction, leading to an increased tethering of SMRT to the RARβ2 promoter, decreased histone acetylation, down-regulation of the RARβ2 expression, and impaired cellular differentiation in response to retinoid. The phosphoinositide 3-kinase/Akt signaling pathway, an important modulator of cellular survival, has thus a direct impact on cellular retinoid sensitivity, and its deregulation may be the triggering event in retinoid resistance of cancer cells.
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Orozco Reina Agustina, Agüero Rocio, Razzeto Gabriela, Gimenez Maria Sofia, and Vasquez Gomez Miriam Ester. "Alterations in oxidative metabolism in liver of female rats: Effects of long-term vitamin A deficiency." GSC Biological and Pharmaceutical Sciences 13, no. 1 (November 30, 2020): 267–78. http://dx.doi.org/10.30574/gscbps.2020.13.1.0064.
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Background: The latest estimate by 5 UN agencies is that 821 million people globally are undernourished, which puts them at risk of vitamin and other nutrient deficiencies. Vitamin A deficiency remains a widespread public health problem among women and children in the developing world the role of vitamin A and its active metabolites in pathways involved in antioxidant protection and in the inhibition of important pathways that promote oxidative stress. Objectives: Determine if vitamin A deficiency could influence oxidative metabolism in 6-month-old female wistar rats. Materials and Methods: Determine the concentration of carbonyl proteins, as a marker of protein oxidation; TBARS, as a lipoperoxidation marker; and nitrotyrosine as a marker of oxidative stress dependent on nitric oxide. Quantify the expression of CAT, SOD, eNOS and iNOS in the liver and wistar rats deficient in vitamin A for 6 months. Results: An increase in the concentration of carbonyl protein and nitrotyrosine in the liver tissue deficient in vitamin A is observed. The expression of SOD, eNOS and iNOS decreased in the group with a private diet of vitamin A. From the regression analysis a positive correlation was established between hepatic retinoic acid levels and gene expression of eNOS, iNOS and SOD. A positive correlation between serum retinoic acid levels and gene expression of eNOS and iNOS was also observed. Conclusions: It is possible to ratify the relationship between the development of stress and vitamin A levels; improving the understanding of hepatic metabolism and its response to the absence of this vitamin.
Dissertations / Theses on the topic "Deficiency; Retinoid pathway gene expression"
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Sokolova, Natalia Valerievna. "The role of vitamin A in embryonic lung development in mice." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320687.
Full textBooks on the topic "Deficiency; Retinoid pathway gene expression"
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Methylation pathway perturbations with folate deficiency: A role for epigenetics in endothelial gene expression. Ottawa: National Library of Canada, 2003.
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