Transcriptomic comparison of the vitamin A ester retinyl propionate and retinol in human keratinocytes
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PROVIDER: PRJNA655636 | ENA |
REPOSITORIES: ENA
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Project description:Retinoids are potent skin care actives used to treat a number of common clinical and cosmetic skin conditions, including skin aging. Here, we compare the effects of retinyl proprionate and retinol on gene expression in immortalized human keratinocytes.
2021-09-09 | GSE155789 | GEO
Project description:We used microarrays to examine the temporal transcriptome changes of vitamin a deficient rats testes replenished with retinol 20-day old rats were put on a vitamin A deficient diet, after nine weeks the animals were treated with retinol for 0-(VAD), 4-, 8-, 24-hr to determine the global transcriptome changes induced by retinol replenishment of the vitmain A deficient testis
2009-02-27 | E-GEOD-14962 | biostudies-arrayexpress
Project description:We used microarrays to examine the temporal transcriptome changes of vitamin a deficient rats testes replenished with retinol
2009-02-27 | GSE14962 | GEO
Project description:Diabetic cardiomyopathy (DCM) is a primary myocardial injury induced by diabetes mellitus (DM) with a complex pathogenesis. In this study, we identified disordered cardiac retinol metabolism in T2DM mice and patients characterized by retinol (vitamin A, Rol) overload, all-trans retinoic acid (atRA) deficiency and retinoic acid receptors (RARs) reduction, and demonstrated that both cardiac Rol overload and atRA deficiency promote DCM by supplementing T2DM mice with Rol or atRA. Mechanically, by constructing cardiomyocyte-specific conditional RDH10-knockout mice and overexpressing RDH10 in T2DM mice via adeno-associated virus, we verified that the reduction in cardiac retinol dehydrogenase 10 (RDH10) is the initiating factor for cardiac retinol metabolism disorder and its resulting DCM. Additionally, lipotoxicity and ferroptosis contribute to the effect of retinol metabolism disorder on DCM. Based on these results, we suggest that the reduction of cardiac RDH10 and its mediated disorder of cardiac retinol metabolism is a new mechanism underlying DCM.
2023-01-15 | GSE202418 | GEO
Project description:Vitamin B12 depletion or propionate supplementation can reverse the transcriptomic aberration in the C. elegans model of PD with neuronal overexpression of alpha-synuclein A53T
2023-04-28 | GSE230786 | GEO
Project description:Vitamin A (retinol) is an essential precursor for the production of retinoic acid (RA), which in turn is a major regulator of gene expression, affecting cell differentiation throughout the body. Understanding how vitamin A nutritional status, as well as therapeutic retinoid treatment, regulates the expression of retinoid homeostatic genes is important for improving dietary recommendations and therapeutic strategies using retinoids. This study investigated genes central to processes of retinoid uptake and storage, release to plasma, and oxidation in the liver of rats under steady-state conditions after different exposures to dietary vitamin A (deficient, marginal, adequate and supplemented), and acutely after administration of a therapeutic dose of all-trans-RA. Over a very wide range of dietary vitamin A, lecithin:retinol acyltransferase (LRAT) as well as multiple cytochrome P450s (CYP26A1, CYP26B1, and CYP2C22) differed by diet and were highly correlated with one another and with vitamin A status assessed by liver retinol concentration (all correlations, P<0.05). After acute treatment with RA, the same genes were rapidly and concomitantly induced, preceding RARß, a classical direct target of RA. CYP26A1 mRNA exhibited the greatest dynamic range (change of log26 in 3 h). Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naïve rats. By in situ hybridization, CYP26A1 mRNA was strongly regulated within hepatocytes, closely resembling RBP4 in location. Overall, whether RA is produced endogenously from retinol or administered exogenously, changes in retinoid homeostatic gene expression simultaneously favor both retinol esterification and RA oxidation, with CYP26A1 exhibiting the greatest dynamic change.
2011-09-01 | GSE24104 | GEO
Project description:Vitamin A (retinol) is an essential precursor for the production of retinoic acid (RA), which in turn is a major regulator of gene expression, affecting cell differentiation throughout the body. Understanding how vitamin A nutritional status, as well as therapeutic retinoid treatment, regulates the expression of retinoid homeostatic genes is important for improving dietary recommendations and therapeutic strategies using retinoids. This study investigated genes central to processes of retinoid uptake and storage, release to plasma, and oxidation in the liver of rats under steady-state conditions after different exposures to dietary vitamin A (deficient, marginal, adequate and supplemented), and acutely after administration of a therapeutic dose of all-trans-RA. Over a very wide range of dietary vitamin A, lecithin:retinol acyltransferase (LRAT) as well as multiple cytochrome P450s (CYP26A1, CYP26B1, and CYP2C22) differed by diet and were highly correlated with one another and with vitamin A status assessed by liver retinol concentration (all correlations, P<0.05). After acute treatment with RA, the same genes were rapidly and concomitantly induced, preceding RARß, a classical direct target of RA. CYP26A1 mRNA exhibited the greatest dynamic range (change of log26 in 3 h). Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naïve rats. By in situ hybridization, CYP26A1 mRNA was strongly regulated within hepatocytes, closely resembling RBP4 in location. Overall, whether RA is produced endogenously from retinol or administered exogenously, changes in retinoid homeostatic gene expression simultaneously favor both retinol esterification and RA oxidation, with CYP26A1 exhibiting the greatest dynamic change. All rats were housed in a room maintained at 22°C with a 12-h dark:light cycle, and food and water were freely available. For the Steady-State Vitamin A Study (experiment 1) and the Retinoic Acid 16-hour Kinetic Study (experiment 2), lactating female Sprague-Dawley rats with 12 female pups (purchased from Charles River Laboratories, Willmington, MA) were fed a vitamin A-deficient purified diet [AIN-93G diet, prepared by Research Diets, New Brunswick, NJ] to reduce the transfer of vitamin A in milk from mother to pups prior to the start of the study. For experiment 1, from weaning, the offspring were fed the same diet modified to contain vitamin A at one of four levels: 0 (vitamin A deficient), 0.4 mg retinol/kg diet (vitamin A marginal), 4 mg retinol/kg diet (vitamin A adequate control), or 100 mg retinol/kg diet (vitamin A supplemented). All rats were studied at 8 weeks of age. Rats were euthanized by carbon dioxide asphyxiation and blood and liver were collected rapidly and frozen in liquid nitrogen for storage at -80°C before analysis. In experiment 2, at 8 weeks of age female vitamin A-deficient rats were treated with ~100 ug of All-trans-Retinoic acid (at-RA) for 0 (vehicle only), 3, 6, 10 or 16 h (n=3-4/group). Tissues were collected and RNA was prepared in the same manner as in experiment 1. In the 90-minute "first pass" kinetic study (experiment 3), female rats were purchased at 6 weeks of age and fed a stock rodent diet. When the rats were 8 weeks old they were assigned to a control (naïve) group. Rats in the naive group received an equal amount of vehicle only (vegetable oil/5% ethanol). Food was removed immediately. Sixteen hours after priming, each rat was lightly anesthetized by isoflurane-oxygen inhalation and treated with ~25 ug all-trans-RA bound to albumin [10 ug RA per 100 g bo dy weight], injected into the exposed left common iliac vein. The incision was closed with a surgical staple. The rats were allowed to recover from the anesthesia. Rats were killed at 0 minute (vehicle injection), and 30, 60, and 90 min (n = 3/group) after injection of the RA test dose. Rats were euthanized by carbon dioxide asphyxiation and blood and liver were collected rapidly and frozen in liquid nitrogen for storage at -80°C before analysis. For experiment 1, five biological repeats were Vitamin A deficient, seven biological repeats were Vitamin A marginal, six biological repeats were Vitamin A adequate, and two biological repeats were Vitamin A supplemented. In experiment 2, three biological repeats were performed for each of the following treatments: untreated, at-RA for 3 hours, at-RA for 6 hours and at-RA for 16 hours. Four biological repeats were treated with at-RA for 10 hours. For experiment 3, two biological repeats were untreated and three biological repeats were performed for each of the following at-RA treatment times: 30, 60 and 90 minutes. A total of 47 samples were analyzed.
2011-08-31 | E-GEOD-24104 | biostudies-arrayexpress
Project description:Retinol Dehydrogenase 10 Reduction Mediated Retinol Metabolism Disorder Promotes Diabetic Cardiomyopathy
| PRJNA835885 | ENA
Project description:Microbiota-derived short chain fatty acids (SCFAs) are one of the hottest issues for its various bioactivities in the gut, immune system extending to brain or other organs through several axises. Though many intensive studies have been implementing til recent, some parts among a plenty of actions occurred in the gut solely are unrevealed so as their mechanism. Propionate, one of the representative SCFAs with butyrate is basically known for its inhibiting activity of histone deacetylation (HDAC) and stimulation of mucin expression in mucosae. However, the mechanism of the stimulating action needs to be elucidated in more detail and understandable way. Here, we firstly investigated the effect of propionate on expression of MUC2, one of the main subtype mucin, in goblet cell line LS 174T and suggest a mechanism of the action along the order of events, linked to metabolic shift. Propionate at the concentration of 1 mM to 4 mM induced the expression of MUC2 gradually in the transcriptional- and protein level at 24 h. At the initial parts of treatment of propionate, the odd SCFA was metabolized along vitamin B12-independent β-oxidation-like pathway and the metabolism led cells to boost mitochondrial respiration until 18 h after treatment. However, another possible metabolism pathway, vitamin B12-dependent carboxylation pathway was not involved to the resulted action. At the latter parts, the master regulator of hypoxia, Hypoxia-induced factors (HIFs) were fluctuated respectively and among them, activated HIF-2α was identified to regulate the expression level of MUC2. In summary, propionate might induce β-oxidation-like pathway at the initial part so that mitochondrial respiration is upregulated. In an effort of LS 174T to adapt to naturally formed hypoxia by response to propionate, each activity of HIF subtypes was regulated in a way of entangled to each other and activated HIF-2α stimulated MUC2 expression.
2024-04-08 | GSE157016 | GEO
Project description:Propionate is an abundant carboxylic acid in nature. Microorganisms metabolize propionate aerobically via the 2-methylcitrate pathway. This pathway depends on a series of three reactions in the citric acid cycle that leads to the conversion of succinate to oxaloacetate. Interestingly, the gamma-proteobacterium Escherichia coli can use propionate as a carbon and electron source under oxic but not under anoxic conditions. The typical downregulation of the citric acid cycle under anoxic conditions is only partially responsible for the inability to use propionate under anoxic conditions since an arcA mutant shows very limited growth on propionate. RT-PCR and transcriptomic analysis revealed a post-transcriptional regulation of the prp-genecluster encoding the necessary enzymes for propionate metabolism. The polycistronic mRNA was hydrolyzed in the 3`-5` direction under anoxic conditions. This regulatory strategy is highly constructive because the last gene of the operon encodes the first enzyme of the propionate metabolism. Further analysis revealed that RNase R catalyzes the hydrolysis of the prp transcripts. Consequently, an rnr-deletion strain could metabolize propionate under anoxic conditions. To the best of our knowledge, this is the first study describing the influence of RNase R on the anaerobic metabolism of E. coli.
2017-12-14 | GSE78814 | GEO