Differentiation-dependent regulation of retinal dehydrogenase gene expression in the trachea

1998 ◽  
Vol 76 (1) ◽  
pp. 59-62 ◽  
Author(s):  
Pangala V Bhat ◽  
Thomas Bader ◽  
Paul Nettesheim ◽  
Anton M Jetten
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Epithelial Cells ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Squamous Metaplasia ◽  
Tracheal Epithelium ◽  
Dehydrogenase Gene ◽  
Retinal Dehydrogenase ◽  
Mucociliary Differentiation

Retinoic acid (RA), a metabolite of vitamin A, is known to be a key signaling molecule in regulating epithelial cell differentiation. We recently characterized and cloned a retinal dehydrogenase (RALDH) that catalyzes the oxidation of retinal to RA. In this study, we investigated the effects of retinoids on the level of RALDH mRNA and protein as well as RALDH activity in the trachea and cultured tracheal epithelial cells. Vitamin A deficiency induced squamous metaplasia in the tracheal epithelium and down-regulated RALDH expression. Supplementation of retinol and retinoic acid to vitamin A deficient rats restored the normal mucociliary epithelium and up-regulated the RALDH expression. In rat epithelial cells cultured in vitro, RAinhibited squamous differentiation and promoted mucociliary differentiation. Squamous differentiated cultures (RA-) expressed very low levels of RALDH mRNA, whereas mucociliary differentiated cultures (RA+) expressed high levels of RALDH mRNA. Retinal and retinol were poor inducers of mucociliary differentiation as well as RALDH expression. The RALDH expression paralleled the expression of the mucin-1 gene in mucociliary cultures. These results suggest that the expression of RALDH is dependent on the differentiation state of the airway epithelium.Key words: retinoic acid, retinal dehydrogenase, gene expression, tracheal epithelium.

scholarly journals Alterations in oxidative metabolism in liver of female rats: Effects of long-term vitamin A deficiency

2020 ◽  
Vol 13 (1) ◽  
pp. 267-278
Author(s):  
Orozco Reina Agustina ◽  
Agüero Rocio ◽  
Razzeto Gabriela ◽  
Gimenez Maria Sofia ◽  
Vasquez Gomez Miriam Ester
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Retinoic Acid ◽  
Vitamin A ◽  
Oxidative Metabolism ◽  
Wistar Rats ◽  
Vitamin A Deficiency ◽  
Female Rats ◽  
Positive Correlation ◽  
Stress Dependent

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.

The Effect of Vitamin A Supplementation on Retinoic Acid-Related Orphan Receptor γt (RORγt) and Interleukin-17 (IL-17) Gene Expression in Avonex-Treated Multiple Sclerotic Patients

2013 ◽  
Vol 51 (3) ◽  
pp. 749-753 ◽  
Author(s):  
Niyaz Mohammadzadeh Honarvar ◽  
Mohammad Hossein Harirchian ◽  
Fariba Koohdani ◽  
Feridoun Siassi ◽  
Mina Abdolahi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Vitamin A ◽  
Orphan Receptor ◽  
Interleukin 17 ◽  
Vitamin A Supplementation

scholarly journals Cellular basis of urothelial squamous metaplasia

2005 ◽  
Vol 171 (5) ◽  
pp. 835-844 ◽  
Author(s):  
Feng-Xia Liang ◽  
Maarten C. Bosland ◽  
Hongying Huang ◽  
Rok Romih ◽  
Solange Baptiste ◽  
...  
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Squamous Metaplasia ◽  
Culture Conditions ◽  
Growth Potential ◽  
Basal Cells ◽  
Cellular Basis ◽  
Proximal Urethra

Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency. Moreover, these cells remain phenotypically distinct even after they have been serially passaged under identical culture conditions, thus ruling out local mesenchymal influence as the sole cause of their in vivo differences. During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium. These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia.

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.

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