scholarly journals Triiodothyronine administration reverses vitamin A deficiency-related hypo-expression of retinoic acid and triiodothyronine nuclear receptors and of neurogranin in rat brain

2003 ◽  
Vol 90 (1) ◽  
pp. 191-198 ◽  
Author(s):  
Marianne Husson ◽  
Valérie Enderlin ◽  
Serge Alfos ◽  
Catherine Féart ◽  
Paul Higueret ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Nuclear Receptors ◽  
Target Gene ◽  
Vitamin A Deficiency ◽  
Deficient Diet ◽  
Neuronal Protein ◽  
Knowing That ◽  
The Brain

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.

Complex regulation of TGF beta expression by retinoic acid in the vitamin A-deficient rat

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1081-1086 ◽  
Author(s):  
A.B. Glick ◽  
B.K. McCune ◽  
N. Abdulkarem ◽  
K.C. Flanders ◽  
J.A. Lumadue ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Alveolar Epithelium ◽  
Tgf Beta ◽  
Basal Expression ◽  
Beta 2 ◽  
Complex Regulation ◽  
First Time

We report the results of a histochemical study, using polyclonal antipeptide antibodies to the different TGF beta isoforms, which demonstrates that retinoic acid regulates the expression of TGF beta 2 in the vitamin A-deficient rat. Basal expression of TGF beta 2 diminished under conditions of vitamin A deficiency. Treatment with retinoic acid caused a rapid and transient induction of TGF beta 2 and TGF beta 3 in the epidermis, tracheobronchial and alveolar epithelium, and intestinal mucosa. Induction of TGF beta 1 expression was also observed in the epidermis. In contrast to these epithelia, expression of the three TGF beta isoforms increased in vaginal epithelium during vitamin A deficiency, and decreased following systemic administration of retinoic acid. Our results show for the first time the widespread regulation of TGF beta expression by retinoic acid in vivo, and suggest a possible mechanism by which retinoics regulate the functions of both normal and pre-neoplastic epithelia.

scholarly journals Utilization of DR1 as true RARE in regulating the Ssm, a novel retinoic acid-target gene in the mouse testis

2007 ◽  
Vol 192 (3) ◽  
pp. 539-551 ◽  
Author(s):  
Kyuyong Han ◽  
Haengseok Song ◽  
Irene Moon ◽  
Robert Augustin ◽  
Kelle Moley ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Nuclear Receptors ◽  
Promoter Region ◽  
Target Gene ◽  
Mouse Testis ◽  
Specific Marker ◽  
Specific Response ◽  
Response Elements

Various nuclear receptors form dimers to activate target genes via specific response elements located within promoters or enhancers. Retinoid X receptor (RXR) serves as a dimerization partner for many nuclear receptors including retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR). Dimers show differential preference towards directly repeated response elements with 1–5 nucleotide spacing, and direct repeat 1 (DR1) is a promiscuous element which recruits RAR/RXR, RXR/RXR, and PPAR/RXR in vitro. In the present investigation, we report identification of a novel RAR/RXR target gene which is regulated by DR1s in the promoter region. This gene, namely spermatocyte-specific marker (Ssm), recruits all the three combinations of nuclear receptors in vitro, but in vivo regulation is observed by trans-retinoic acid-activated RAR/RXR dimer. Indeed, chromatin immunoprecipitation experiment demonstrates binding of RARβ and RXRα in the promoter region of the Ssm. Interestingly, expression of Ssm is almost exclusively observed in spermatocytes in the adult mouse testis, where RA signaling is known to regulate developmental program of male germ cells. The results show that Ssm is a RAR/RXR target gene uniquely using DR1 and exhibits stage-specific expression in the mouse testis with potential function in later stages of spermatogenesis. This finding exemplifies usage of DR1s as retinoic acid response element (RARE) under a specific in vivo context.

Vitamin A deficiency in mice causes a systemic expansion of myeloid cells

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3349-3356 ◽  
Author(s):  
Takeshi Kuwata ◽  
I-Ming Wang ◽  
Tomohiko Tamura ◽  
Roshini M. Ponnamperuma ◽  
Rachel Levine ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Cell Population ◽  
Vitamin A Deficiency ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Direct Result ◽  
Essentially Normal ◽  
Deficient Mice

Abstract To examine the role of retinoids in hematopoietic cell growth in vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient mice exhibited a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. The abnormal expansion of myeloid cells was detected from an early stage of vitamin A deficiency and contrasted with essentially normal profiles of T and B lymphocytes. This abnormality was reversed on addition of retinoic acid to the vitamin A–deficient diet, indicating that the myeloid cell expansion is a direct result of retinoic acid deficiency. TUNEL analysis indicated that spontaneous apoptosis, a normal process in the life cycle of myeloid cells, was impaired in vitamin A–deficient mice, which may play a role in the increased myeloid cell population. Quantitative reverse transcriptase-polymerase chain reaction analysis of purified granulocytes showed that expression of not only RAR, but RXRs, 2 nuclear receptors that mediate biologic activities of retinoids, was significantly reduced in cells of deficient mice. This work shows that retinoids critically control the homeostasis of myeloid cell population in vivo and suggests that deficiency in this signaling pathway may contribute to various myeloproliferative disorders.

Vitamin A deficiency in mice causes a systemic expansion of myeloid cells

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3349-3356 ◽  
Author(s):  
Takeshi Kuwata ◽  
I-Ming Wang ◽  
Tomohiko Tamura ◽  
Roshini M. Ponnamperuma ◽  
Rachel Levine ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Cell Population ◽  
Vitamin A Deficiency ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Direct Result ◽  
Essentially Normal ◽  
Deficient Mice

To examine the role of retinoids in hematopoietic cell growth in vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient mice exhibited a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. The abnormal expansion of myeloid cells was detected from an early stage of vitamin A deficiency and contrasted with essentially normal profiles of T and B lymphocytes. This abnormality was reversed on addition of retinoic acid to the vitamin A–deficient diet, indicating that the myeloid cell expansion is a direct result of retinoic acid deficiency. TUNEL analysis indicated that spontaneous apoptosis, a normal process in the life cycle of myeloid cells, was impaired in vitamin A–deficient mice, which may play a role in the increased myeloid cell population. Quantitative reverse transcriptase-polymerase chain reaction analysis of purified granulocytes showed that expression of not only RAR, but RXRs, 2 nuclear receptors that mediate biologic activities of retinoids, was significantly reduced in cells of deficient mice. This work shows that retinoids critically control the homeostasis of myeloid cell population in vivo and suggests that deficiency in this signaling pathway may contribute to various myeloproliferative disorders.

Expression of Retinoic Acid Nuclear Receptors and Tissue Transglutaminase Is Altered in Various Tissues of Rats Fed a Vitamin A-Deficient Diet

1992 ◽  
Vol 122 (11) ◽  
pp. 2144-2152 ◽  
Author(s):  
Ajit K. Verma ◽  
Alex Shoemaker ◽  
Ruby Simsiman ◽  
Mitchell Denning ◽  
Richard D. Zachman
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Nuclear Receptors ◽  
Tissue Transglutaminase ◽  
Deficient Diet

scholarly journals The retinol requirements of rats for spermatogenesis and vision

1969 ◽  
Vol 23 (3) ◽  
pp. 619-626 ◽  
Author(s):  
W.A. Coward ◽  
J.McC. Howell ◽  
J.N. Thompson ◽  
G. A. J. PITT
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Beneficial Effect ◽  
General Health ◽  
Vitamin A Deficiency ◽  
Experimental Period ◽  
Normal Vision ◽  
Retinyl Acetate ◽  
Deficient Diet ◽  
Histological Appearance

1. Hooded rats were fed from weaning on a basal retinol-deficient diet containing retinoic acid. Such a diet maintains growth and general health but does not prevent the appearance of lesions associated with vitamin A deficiency in the retina and testis. Some animals were also given supplements of retinol averaging 0.1, 0.25, 1 or 5 μg retinyl acetate per day. Rats were killed at intervals up to 28 weeks after weaning. The weights of the testes and the histological appearance of the testes and epididymides indicated that 5 μg retinyl acetate per day had maintained spermatogenesis throughout the experimental period. Doses averaging 1 μg retinyl acetate per day were only partially effective and the two smaller doses had little beneficial effect.2. In a second similar experiment rats were given doses of retinyl acetate averaging 0.25, 0.5, 1, 2 or 100 μg per day. Measurements of the electroretinogram thresholds of the rats indicated that a dose of 1 μg retinyl acetate per day maintained mainly normal vision until the end of the experiment 29 weeks after weaning. Additional histological observations made 21 weeks after weaning showed that this dose level had not maintained spermatogenesis but that doses of 2 μg retinyl acetate per day had been effective.3. The experiments show that the differing functions of vitamin A in spermatogenesis and vision are reflected in the hooded rat in differences in the dietary retinol levels needed to maintain these processes.

Effects of retinoic acid on the concentrations of radioactive metabolites of retinol in tissues of rats maintained on a retinol-deficient diet

1991 ◽  
Vol 69 (6) ◽  
pp. 826-830 ◽  
Author(s):  
Pangala V. Bhat ◽  
André Lacroix
Keyword(s):  
High Performance Liquid Chromatography ◽  
Retinoic Acid ◽  
Vitamin A ◽  
High Performance ◽  
Vitamin A Deficiency ◽  
Kidney Tissue ◽  
Experimental Period ◽  
Deficient Diet ◽  
Retinyl Ester ◽  
Effect Of Feeding

The effect of feeding retinoic acid for 2 and 6 days on the metabolism of labeled retinol in tissues of rats maintained on a vitamin A deficient diet was studied. The metabolites of retinol were analyzed by high performance liquid chromatography. Feeding retinoic acid for 2 days significantly reduced the blood retinol and retinyl ester levels without affecting the vitamin A content of the liver. In intestine and testis the content of labeled retinoic acid was decreased significantly by dietary retinoic acid. Addition of retinoic acid to the diet for 6 days resulted, in addition to decreased blood retinol and retinyl ester values, in an increase in the retinyl ester values in the liver. The accumulation of retinyl ester in the retinoic acid fed rat liver was accompanied by an absence of labeled retinoic acid. Kidney tissue was found to contain the highest levels of labeled retinoic acid, retinol, and retinyl esters; dietary retinoic acid did not alter the concentrations of these retinoids in the kidney during the experimental period. Since kidney retained more vitamin A when the liver vitamin A was low and also dietary retinoic acid did not affect the concentrations of radioactive retinoic acid in the kidney, it is suggested that the kidney may play a major role in the production of retinoic acid from retinol in the body.Key words: retinol, retinoic acid, vitamin A deficiency, tissue metabolites, rat.

Vitamin A and Retinoic Acid in Cognition and Cognitive Disease

2020 ◽  
Vol 40 (1) ◽  
pp. 247-272 ◽  
Author(s):  
Marta U. Wołoszynowska-Fraser ◽  
Azita Kouchmeshky ◽  
Peter McCaffery
Keyword(s):  
Retinoic Acid ◽  
Synaptic Plasticity ◽  
Vitamin A ◽  
Cognitive Decline ◽  
Developmental Disorders ◽  
Vitamin A Deficiency ◽  
Retinoic Acid Receptors ◽  
Controlled Synthesis ◽  
History Of ◽  
The Brain

The history of vitamin A goes back over one hundred years, but our realization of its importance for the brain and cognition is much more recent. The brain is more efficient than other target tissues at converting vitamin A to retinoic acid (RA), which activates retinoic acid receptors (RARs). RARs regulate transcription, but their function in the cytoplasm to control nongenomic actions is also crucial. Controlled synthesis of RA is essential for regulating synaptic plasticity in regions of the brain involved in learning and memory, such as the hippocampus. Vitamin A deficiency results in a deterioration of these functions, and failure of RA signaling is perhaps associated with normal cognitive decline with age as well as with Alzheimer's disease. Further, several psychiatric and developmental disorders that disrupt cognition are also linked with vitamin A and point to their possible treatment with vitamin A or RA.

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