scholarly journals Retinal dehydrogenase gene expression in stomach and small intestine of rats during postnatal development and in vitamin A deficiency

FEBS Letters ◽  
1998 ◽  
Vol 426 (2) ◽  
pp. 260-262 ◽  
Author(s):  
Pangala V. Bhat
1998 ◽  
Vol 76 (1) ◽  
pp. 59-62 ◽  
Author(s):  
Pangala V Bhat ◽  
Thomas Bader ◽  
Paul Nettesheim ◽  
Anton M Jetten

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.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Zhi Chai ◽  
Yafei Lyu ◽  
Qiuyan Chen ◽  
Cheng-Hsin Wei ◽  
Lindsay Snyder ◽  
...  

Abstract Objectives To characterize and compare the impact of vitamin A (VA) deficiency on gene expression patterns in the small intestine (SI) and the colon, and to discover novel target genes in VA-related biological pathways. Methods vitamin A deficient (VAD) mice were generated by feeding VAD diet to pregnant C57/BL6 dams and their post-weaning offspring. Total mRNA extracted from SI and colon were sequenced using Illumina HiSeq 2500 platform. Differentially Expressed Gene (DEG), Gene Ontology (GO) enrichment, and Weighted Gene Co-expression Network Analysis (WGCNA) were performed to characterize expression patterns and co-expression patterns. Results The comparison between vitamin A sufficient (VAS) and VAD groups detected 49 and 94 DEGs in SI and colon, respectively. According to GO information, DEGs in the SI demonstrated significant enrichment in categories relevant to retinoid metabolic process, molecule binding, and immune function. Immunity related pathways, such as “humoral immune response” and “complement activation,” were positively associated with VA in SI. On the contrary, in colon, “cell division” was the only enriched category and was negatively associated with VA. WGCNA identified modules significantly correlated with VA status in SI and in colon. One of those modules contained five known retinoic acid targets. Therefore we have prioritized the other module members (e.g., Mbl2, Mmp9, Mmp13, Cxcl14 and Pkd1l2) to be investigated as candidate genes regulated by VA. Comparison of co-expression modules between SI and colon indicated distinct VA effects on these two organs. Conclusions The results show that VA deficiency alters the gene expression profiles in SI and colon quite differently. Some immune-related genes (Mbl2, Mmp9, Mmp13, Cxcl14 and Pkd1l2) may be novel targets under the control of VA in SI. Funding Sources NIH training grant and NIH research grant. Supporting Tables, Images and/or Graphs


2000 ◽  
Vol 41 (4) ◽  
pp. 410-415 ◽  
Author(s):  
Z. Uni ◽  
G. Zaiger ◽  
O. Gal-Garber ◽  
M. Pines ◽  
I. Rozenboim ◽  
...  

1994 ◽  
Vol 106 (5) ◽  
pp. 1223-1232 ◽  
Author(s):  
Edmond H.H.M. Rings ◽  
Stephen D. Krasinski ◽  
Erik H. Van Beers ◽  
Antoon F.M. Moorman ◽  
Jan Dekker ◽  
...  

Nutrition ◽  
2009 ◽  
Vol 25 (7-8) ◽  
pp. 828-838 ◽  
Author(s):  
Verónica Analía Vega ◽  
Ana Cecilia Anzulovich ◽  
Silvia Mabel Varas ◽  
Mirtha Ruth Bonomi ◽  
María Sofía Giménez ◽  
...  

1998 ◽  
Vol 80 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Zehava Uni ◽  
Gidi Zaiger ◽  
Ram Reifen

The effect of vitamin A on chicken intestinal mucosal morphology and functionality was tested in relation to severe and mild vitamin A deficiency and vitamin A repletion. Compared with rats and mice, chickens have a very quick response to a deficient dietary intake. Severe vitamin A deficiency altered the small intestine of chickens at both the biochemical and the morphological levels. It caused the loss of mucosal protein, reduced villus height and crypt depth and diminished activities of disaccharidases, transpeptidase and alkaline phosphate (EC 3.1.3.1). The ratios RNA-.DNA, RNA:protein and protein:DNA, and the DNA concentrations in 1 g intestinal tissue, together with morphological measurements, provided knowledge about the pattern of lesion. The results indicated that (1) lack of vitamin A influenced cellular hyperplasia as it caused an increase in DNA content and in the number of enterocytes per villus; (2) lack of vitamin A influenced cellular hypertrophy as it decreased the protein:DNA ratio. There was no difference in mucosal enzyme activity between the two deficient groups. The repletion group exhibited a remarkable increase in mucosal enzyme activity only 4 d after switching to the control diet. The evidence presented in our paper suggests that the low vitamin A supply interferes with the normal activity of chicken intestinal mucosa as it influences the processes of proliferation and maturation of enterocytes.


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