Expression Patterns of Class I and Class IV Alcohol Dehydrogenase Genes in Developing Epithelia Suggest a Role for Alcohol Dehydrogenase in Local Retinoic Acid Synthesis

Ang, Hwee Luan; Deltour, Louise; Zgombic-Knight, Mirna; Wagner, Michael; Duester, Gregg

doi:10.1111/j.1530-0277.1996.tb01946.x

Cited by 81 publications

(63 citation statements)

References 56 publications

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“…2). Ang et al reported tissue expression and localization of ADH class I gene and class IV gene in mice and their results were compatible to our results [15]. Vertebrate ADHs consist of a family of cytosolic enzymes divided into eight classes.…”

Section: Discussionsupporting

confidence: 81%

“…Crystal structures of ADH class I and class IV revealed a conserved active site that can accommodate long chain alcohols such as retinol [18][19][20]. ADH class I is expressed at high levels in many retinoid target tissues of embryos [15,21] and in adult epithelia, such as intestine, kidney, adrenal gland, testis, epididymis, uterus and ovary [15,[22][23][24][25]. Retinoid signaling is thought to function in an autocrine or paracrine fashion via the local production of RA at the site of action.…”

Section: Discussionmentioning

confidence: 99%

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Evidence for the Expression of Alcohol Dehydrogenase Class I Gene in Rat Uterus and Its Up-regulation by Progesterone

et al. 2008

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Abstract. The endometrium is one of the target tissues of the ovarian steroid hormones, estrogen and progesterone. In order to elucidate the mechanism of gene regulation in the endometrium, suppressive subtraction hybridization was performed to isolate the candidate genes controlled by progesterone in rat uterus. Alcohol dehydrogenase (ADH) class I gene was one of the candidate genes. Here we investigated the expression and regulation of ADH class I gene in rat uterus. The mRNA of ADH class I was detected in uterus by RT-PCR using specific primers. Using specific probe for ADH class I, in situ hybridization was performed to investigate localization in rat uterus. Positive signals were detected in the endometrial stromal cells of rat uterus by in situ hybridization and were not detected in endometrial epithelial cells and myometrium in rat uterus. Ovariectomized rats were treated with 17-β estradiol and progesterone and the uteri of these rats were used for Northern blot analysis and assay of the ADH activity. Northern blot analysis revealed that the expression of ADH class I mRNA in rat uteri was up-regulated approximately two-fold after progesterone treatment, but not estrogen. Likewise, ADH activity was approximately two-fold higher in progesterone-treated rat uteri compared with controls. This study demonstrated that ADH class I gene is progesterone-responsive in the uterus. This implies that progesterone might be involved with retinoic acid synthesis in the uterus, since ADH is the key enzyme for retinoic acid synthesis.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Evidence for the Expression of Alcohol Dehydrogenase Class I Gene in Rat Uterus and Its Up-regulation by Progesterone

et al. 2008

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“…The expression pattern of RDH4 is only partially overlapping with other known retinoid-metabolizing enzymes expressed in developing embryos (34)(35)(36). At present, the functional implications of this observation is unclear but it may suggest that several different enzymes͞enzyme classes are involved in regulation of RA homeostasis during development.…”

Section: Discussionmentioning

confidence: 81%

The identification of a 9- cis retinol dehydrogenase in the mouse embryo reveals a pathway for synthesis of 9- cis retinoic acid

Romert

Tuvendal

Simon

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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The ligand-controlled retinoic acid (RA) receptors and retinoid X receptors are important for several physiological processes, including normal embryonic development, but little is known about how their ligands, all-trans and 9-cis RA, are generated. Here we report the identification of a stereo-specific 9-cis retinol dehydrogenase, which is abundantly expressed in embryonic tissues known to be targets in the retinoid signaling pathway. The membranebound enzyme is a member of the short-chain alcohol dehydrogenase͞reductase superfamily, able to oxidize 9-cis retinol into 9-cis retinaldehyde, an intermediate in 9-cis RA biosynthesis. Analysis by nonradioactive in situ hybridization in mouse embryos shows that expression of the enzyme is temporally and spatially well controlled during embryogenesis with prominent expression in parts of the developing central nervous system, sensory organs, somites and myotomes, and several tissues of endodermal origin. The identification of this enzyme reveals a pathway in RA biosynthesis, where 9-cis retinol is generated for subsequent oxidation to 9-cis RA.

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“…However, it is not clear why the expression of RALDH declines after birth in the intestine, although there is continuous removal and proliferation of intestinal epithelium occurs during postnatal development [23]. Studies have shown that RA is present in the small intestine of 16.5 dpc embryos and adults [24,25]. Since intestine is one of the main organs involved in retinoid uptake, storage, turnover, and excretion [26], it is possible that adult small intestine may take up RA from the circulation or absorb it from the diet and RA present in the tissue may account for this form of RA and not in situ generated RA.…”

Section: Resultsmentioning

confidence: 99%

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

Bhat

1998

FEBS Letters

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Retinal dehydrogenase (RALDH) catalyzes the oxidation of retinal to all-trans and 9-cis retinoic acid, which function as ligands controlling RAR and RXR nuclear receptorsignaling pathways. We have recently shown the expression of RALDH transcript in the stomach and small intestine by reverse transcription polymerase chain reaction [Bhat, P.V., Labrecque J., Dumas, F., Lacroix, A. and Yoshida, A. (1995) Gene 166, 303^306]. We have examined RALDH expression in the stomach and small intestine before and during postnatal development and in vitamin A deficiency by assaying for mRNA levels and protein as well as for enzyme activity. In 32 day fetuses, RALDH expression was high in the small intestine, whereas RALDH protein was not detectable in the stomach. However, expression of RALDH was seen in the stomach after birth, and gradually increased with age and reached the highest level at postnatal day 42. In the intestine, RALDH expression decreased postnatally. Vitamin A deficiency up-regulated RALDH expression in the stomach and small intestine, and administration of retinoids down-regulated the RALDH expression in these tissues. These results show the differential expression of RALDH in the stomach and small intestine during postnatal development, and that vitamin A status regulates the expression of RALDH gene in these tissues.z 1998 Federation of European Biochemical Societies.

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Expression Patterns of Class I and Class IV Alcohol Dehydrogenase Genes in Developing Epithelia Suggest a Role for Alcohol Dehydrogenase in Local Retinoic Acid Synthesis

Cited by 81 publications

References 56 publications

Evidence for the Expression of Alcohol Dehydrogenase Class I Gene in Rat Uterus and Its Up-regulation by Progesterone

Evidence for the Expression of Alcohol Dehydrogenase Class I Gene in Rat Uterus and Its Up-regulation by Progesterone

The identification of a 9- cis retinol dehydrogenase in the mouse embryo reveals a pathway for synthesis of 9- cis retinoic acid

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

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