Transcriptomic comparison of the vitamin A ester retinyl propionate and retinol in human keratinocytes
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE155789 | GEO | 2021/09/09
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptomic comparison of the vitamin A ester retinyl propionate and retinol in human keratinocytes
| PRJNA655636 | ENA
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:Background: Topical retinoids are effective in retarding skin aging and restoring homeostasis in skin conditions, such as psoriasis. However their adverse effects, which include irritation (retinoid dermatitis), photosensitivity and teratogenicity, limit their use level and patient compliance. Development of a retinoid analogue with minimal adverse effects would allow a broader and more compliant use. Objective: Here we report the synthesis of a novel molecule - bakuchiol salicylate (bakusylan) with the gene expression modulatory profile similar to retinoids, using as reference 3 prescription retinoids - tretinoin, tazarotene and adapalene. Methods: Having a structure entirely different from existing retinoids, we hypothesized that at least a partial uncoupling of retinoid adverse effects from retinoid skin normalizing activity may be obtained with bakuchiol salicylate. This hypothesis was tested in psoriasiform cultures of keratinocytes and organotypic skin substitutes by DNA microarrays and custom PCR arrays. Results: The evaluation of the bioactivity of bakuchiol salicylate revealed the elimination of several components of the retinoid-like proinflammatory response and teratogenic signature without a substantial loss of normalizing potential. A possible mechanism of action consisting in keratinocyte desensitization to cytokine signaling through the inhibition of the STAT1/3/interferon inflammatory signal transduction axis has also been identified. Conclusion: Bipartite materials obtained by merging two skin-active entities with specific, complementary bioactivities, such as bakuchiol and salicylic acid, may deliver a new class of functional retinoids.
2017-03-24 | GSE79642 | 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:Retinol Dehydrogenase 10 Reduction Mediated Retinol Metabolism Disorder Promotes Diabetic Cardiomyopathy
| PRJNA835885 | ENA
Project description:In vivo pathways of natural retinoid metabolism and elimination have not been well characterized in primary myeloid cells, even though retinoids and retinoid receptors have been strongly implicated in regulating myeloid maturation. Using a UAS-GFP reporter transgene, and retrovirally expressed Gal4-RARA in primary mouse bone marrow cells, we identified two distinct enzymatic pathways utilized by mouse myeloid cells ex vivo to synthesize RARA ligands from free vitamin A metabolites (retinyl acetate, retinol, and retinal). Bulk Kit+ bone marrow progenitor cells utilize diethylaminobenzaldehyde (DEAB)-sensitive enzymes, whereas bone marrow-derived macrophages use DEAB-insensitive enzymes to synthesize natural RARA-activating retinoids (all-trans retinoic acid). Bone marrow-derived macrophages do not express the DEAB-sensitive enzymes Aldh1a1, Aldh1a2, or Aldh1a3, but instead express Aldh3b1, which we found is capable of DEAB-insensitive synthesis of all trans-retinoic acid. However, under steady-state and stimulated conditions in vivo, diverse bone marrow cells and peritoneal macrophages showed no evidence of intracellular RARA-activating retinoids despite expression of these enzymes and a vitamin A sufficient diet, suggesting that the enzymatic conversion of retinal is not the rate limiting step in the synthesis of intracellular RARA-activating retinoids in myeloid bone marrow cells and that that RARA remains in an un-liganded configuration during adult hematopoiesis. In order to identify additional enzymes that might contribute to DEAB-insensitive retinoid synthesis in bone marrow-derived macrophages, we compared gene expression in Kit+ progenitor cells vs bone marrow macrophages by Affymetrix array profiling. We analyzed 3 biological samples each of mouse bone marrow-derived macrophages and Kit+ progenitor cells
2015-12-17 | E-GEOD-76060 | biostudies-arrayexpress
Project description:In vivo pathways of natural retinoid metabolism and elimination have not been well characterized in primary myeloid cells, even though retinoids and retinoid receptors have been strongly implicated in regulating myeloid maturation. Using a UAS-GFP reporter transgene, and retrovirally expressed Gal4-RARA in primary mouse bone marrow cells, we identified two distinct enzymatic pathways utilized by mouse myeloid cells ex vivo to synthesize RARA ligands from free vitamin A metabolites (retinyl acetate, retinol, and retinal). Bulk Kit+ bone marrow progenitor cells utilize diethylaminobenzaldehyde (DEAB)-sensitive enzymes, whereas bone marrow-derived macrophages use DEAB-insensitive enzymes to synthesize natural RARA-activating retinoids (all-trans retinoic acid). Bone marrow-derived macrophages do not express the DEAB-sensitive enzymes Aldh1a1, Aldh1a2, or Aldh1a3, but instead express Aldh3b1, which we found is capable of DEAB-insensitive synthesis of all trans-retinoic acid. However, under steady-state and stimulated conditions in vivo, diverse bone marrow cells and peritoneal macrophages showed no evidence of intracellular RARA-activating retinoids despite expression of these enzymes and a vitamin A sufficient diet, suggesting that the enzymatic conversion of retinal is not the rate limiting step in the synthesis of intracellular RARA-activating retinoids in myeloid bone marrow cells and that that RARA remains in an un-liganded configuration during adult hematopoiesis. In order to identify additional enzymes that might contribute to DEAB-insensitive retinoid synthesis in bone marrow-derived macrophages, we compared gene expression in Kit+ progenitor cells vs bone marrow macrophages by Affymetrix array profiling.
2015-12-17 | GSE76060 | GEO
Project description:The skin is the human body’s largest organ and is in contact with a diverse community of microorganisms that includes both resident and pathogenic bacteria. Skin immune defenses include the production of antimicrobial proteins that kill bacteria directly. However, we still have an incomplete understanding of how skin antimicrobial proteins promote homeostasis with resident bacterial communities and limit infection. Here, we show that resistin-like molecule α (RELMα) is an antibacterial protein that is produced by keratinocytes and sebocytes in the mouse skin. RELMα expression was induced in mouse skin by resident and pathogenic skin bacteria and was bactericidal for several bacterial species found on the skin, including Streptococcus pyogenes. Mice lacking RELMα had altered resident skin bacterial communities and were more susceptible to bacterial infection, indicating that RELMα controls bacterial colonization of the skin. RELMα expression required dietary vitamin A and could be induced by therapeutic retinoids that protected against bacterial infection in a RELMα-dependent manner. Resistin, another member of the RELM family, was expressed in human skin, required retinoids for expression, and killed skin bacteria, indicating a conserved function for RELM proteins in skin innate immunity. Our findings thus identify members of the RELM family as antibacterial proteins that provide vitamin A-dependent antimicrobial protection of the skin, and provide insight into why skin immunity requires adequate dietary vitamin A.
2019-04-30 | GSE108718 | 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