Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1088840 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28367340_1.fastq.gz | Fastqsanger.gz | |||
| SRR28367340_2.fastq.gz | Fastqsanger.gz | |||
| SRR28367341_1.fastq.gz | Fastqsanger.gz | |||
| SRR28367341_2.fastq.gz | Fastqsanger.gz | |||
| SRR28367342_1.fastq.gz | Fastqsanger.gz |
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Project description:The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of cultured human immortalized sebocytes (SEB-1) treated with 13-cis RA was performed to gain insights into its sebocyte-specific mechanism of action. SEB-1 sebocytes were cultured with 0.1 uM 13-cis RA for 72 hours or vehicle control. Gene array expression profiling was conducted using Affymetrix HG-U95Av2 arrays in order to examine changes in gene expression as a result of treatment. A total of 85 genes (78 different genes) were significantly influenced by 13-cis RA: 58 were upregulated and 27 were down-regulated. There were changes in several genes involved in apoptosis and innate immunity. These studies are the first describing the sebocyte- specific response in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. Keywords: effects of 72 hour 13-cis RA treatment on cultured human sebocyte cells (SEB-1)
2008-03-04 | GSE10432 | GEO
Project description:The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of cultured human immortalized sebocytes (SEB-1) treated with 13-cis RA was performed to gain insights into its sebocyte-specific mechanism of action. SEB-1 sebocytes were cultured with 0.1 uM 13-cis RA for 72 hours or vehicle control. Gene array expression profiling was conducted using Affymetrix HG-U95Av2 arrays in order to examine changes in gene expression as a result of treatment. A total of 85 genes (78 different genes) were significantly influenced by 13-cis RA: 58 were upregulated and 27 were down-regulated. There were changes in several genes involved in apoptosis and innate immunity. These studies are the first describing the sebocyte- specific response in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. Experiment Overall Design: Total of 6 chips: 3 vehicle (DMSO) control and 3 13-cis RA (0.1 uM) treatment.
2008-04-06 | E-GEOD-10432 | biostudies-arrayexpress
Project description:The retinoic acid (RA) signaling pathway is essential for cardiac development; however, cardiomyocytes, the main cell type of the heart, are considered to be unresposive to RA signaling. The goal of this study was to examine the effects of all-trans RA (atRA) treatment on cardiomyocytes isolated from E18.5 mouse embryos. We found that cardiomyocytes, contrary to previous findings, are indeed repsonsive to RA signaling and that many genes involved in cardiac developmental and repair processes were significantly deregulated upon atRA trearment. These findings have important implications for the heart development and regeneration fields.
2021-04-01 | GSE161429 | GEO
Project description:The cell differentiation potential of 13-cis retinoic acid (RA) has not succeeded in the clinical treatment of glioblastoma (GBM) so far. However, RA may also induce the expression of disistance genes such as HOXB7 which can be suppressed by Thalidomide (THAL). Therefore, we tested if combined treatment with RA+THAL may inhibit growth of glioblastoma in vivo. Treatment with RA+THAL but not RA or THAL alone significantly inhibited tumour growth. The synergistic effect of RA and THAL was corroborated by the effect on proliferation of glioblastoma cell lines in vitro. HOXB7 was not upregulated but microarray analysis validated by real-time PCR identified four potential resistance genes (IL-8, HILDPA, IGFBPA, and ANGPTL4) whose upregulation by RA was suppressed by THAL. Furthermore, genes coding for small nucleolar RNAs (snoRNA) were identified as a target for RA for the first time, and their upregulation was maintained after combined treatment. Pathway analysis showed upregulation of the Ribosome pathway and downregulation of pathways associated with proliferation and inflammation. Combined treatment with RA + THAL delayed growth of GBM xenografts and suppressed putative resistance genes associated with hypoxia and angiogenesis. This encourages further pre-clinical and clinical studies of this drug combination in GBM. The purpose was to study differential gene expression in glioblastoma xenografts after treatment with 13-cis retinoic acid (RA), thalidomide (Thal) or a combination of both drugs.
2015-07-23 | E-GEOD-71224 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series:; GSE10432: 13-cis retinoic acid treatment of human sebocytes (SEB-1); GSE10433: Human Skin: Before and 1 week after Isotretinoin Treatment; The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of cultured human immortalized sebocytes (SEB-1) treated with 13-cis RA was performed to gain insights into its sebocyte-specific mechanism of action. SEB-1 sebocytes were cultured with 0.1 uM 13-cis RA for 72 hours or vehicle control. Gene array expression profiling was conducted using Affymetrix HG-U95Av2 arrays in order to examine changes in gene expression as a result of treatment. A total of 85 genes (78 different genes) were significantly influenced by 13-cis RA: 58 were upregulated and 27 were down-regulated. There were changes in several genes involved in apoptosis and innate immunity. These studies are the first describing the sebocyte- specific response in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of skin from 6 patients treated with isotretinoin was performed to gain insights into its mechanism of action. Skin biopsies were obtained from the patients at baseline and at one-week isotretinoin treatment. Gene array expression profiling was conducted using Affymetrix HG-U133A 2.0 arrays in order to examine changes in gene expression as a result of treatment. After treatment, 43 genes were significantly changed: 38 up-regulated and 5 down-regulated. A significant proportion of these genes are involved in pathways that regulate differentiation, tumor suppression, serine proteases, serine protease inhibitors and solute transfer. These studies are the first describing the initial changes in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. Experiment Overall Design: Refer to individual Series
2008-04-06 | E-GEOD-10434 | biostudies-arrayexpress
Project description:Retinoic acid (RA) is an important developmental signaling molecule responsible for the patterning of multiple vertebrate tissues. RA is also a potent teratogen, causing multi-organ birth defects in humans. Endogenous RA levels must therefore be tightly controlled in the developing embryo. In order to understand the RA function and regulation at the genomic level, we used a microarray approach to identify genes that function as negative feedback regulators of retinoic acid signaling. To that end, we treated embryos with different chemicals: DMSO as control, AGN193019 as RA antagonist at high concentration 10uM and low concentration 1uM, as well as 0.33uM RA. Each treatment has four biological replicates. We screened for genes expressed in early somite-stage embryos that respond oppositely to treatment with RA versus RA antagonists, and validated them by whole-mount RNA in situ hybridization.
2009-05-29 | GSE16264 | GEO
Project description:The whole embryo culture (WEC) model serves as a potential replacement for classical in vivo developmental toxicity testing. In this alternative test, cultured rat embryos are exposed during neurulation and early organogenesis and evaluated for morphological adverse outcomes. Toxicogenomic-based approaches may improve the predictive ability of WEC by providing molecular-based markers associated with chemical exposure which can be compared across multiple parameters (e.g. time, dose, model). Additionally, comparisons between in vitro and in vivo models may identify objective, relevant molecular responses linked with developmental toxicity endpoints in vivo. In this study, using a transcriptomic approach, we compared all-trans-retinoic acid (RA)-exposed and non-exposed Wistar rat embryos derived using WEC (RA, 0.5µg/mL) or in vivo (RA, 50mg/kg, oral gavage) to identify overlapping and non-overlapping effects of RA on RNA expression in parallel with morphological changes. Across six time points (GD 10 + 2-48h), we observed strong similarities in RA-response at the gene (directionality, significance) and functional (e.g. embryonic development, cell differentiation) level which associated with RA-induced adverse morphological effects, including growth reduction as well as alterations of neural tube, limb, branchial, and mandible development. Differences between models in the timing of RA-induced impacts on the expression of select genes related to embryonic development and RA-metabolism associated with specific differential morphological outcomes. This study supports the use of WEC to examine compound-induced molecular responses relative to in vivo, and furthermore, assists in defining the applicability domain of the WEC in determining complementary windows of sensitivity for developmental toxicological investigations. Cultured embryos mimic the morphological developmental progression of embryos (in vivo) undergoing neurulation and early organogenesis. Using available genomics technologies, comparative molecular-based assessments between cultured embryos and in vivo models may further clarify commonalities and dissimilarities which contribute to differences between systems. Therefore, in this study, using a transcriptomic approach, we compared cultured whole rat embryos and embryos in vivo at comparable time points in development (gestational day (GD) 10 + 2-48h, GD 0 = copulatory plug) to assess for commonalities and differences in gene expression in relation to morphology. We reveal strong parallels in time-dependent expression of genes in terms of magnitude, directionality and functionality between whole embryo culture (WEC) and in vivo (rat). Genes changing in expression over time resemble previously hypothesized mechanisms underlying early development in mammalian systems. Furthermore, at the gene and functional level, we identify genes which differ in expression between models, including genes related to development, oxygen transport and metabolism. In summary, our results support the use of WEC for toxicological studies aimed at representing in vivo development during this time-window at the molecular level. Additionally, we indicate genes which differ in expression between models, providing possible insights for improvement of culture conditions.
2012-03-12 | GSE33195 | GEO
Project description:Retinoic acid (RA) functions as a ligand for the nuclear RA receptors (RARs), which regulate the expression of target genes by binding to RA response elements. RA signaling is required for multiple processes during chordate embryonic development, such as body axis extension, hindbrain antero-posterior patterning and forelimb bud initiation. Although some RA target genes have been identified, little is known about the genome-wide effects of RA signaling during in vivo embryonic development. Here we stimulate the RA pathway during development by treating zebrafish embryos with all-trans-RA (atRA), the most abundant form of RA, and use a combination of RNA-seq, ATAC-seq, ChIP-seq and HiChIP to gain insight into the molecular mechanisms by which RA signaling control target gene expression. We find that RA signaling is involved in anterior/posterior patterning and development of the central nervous system, participating in the transition from pluripotency to differentiation. atRA treatment also induces alterations in chromatin accessibility during early development and promotes chromatin binding of RARaa and the RA targets Hoxb1b, Meis2b and Sox3, which cooperate in central nervous system development. Finally, we show that RA induces a rewiring of chromatin architecture, with alterations in chromatin 3D interactions that are consistent with target gene expression. This is illustrated by the specific induction of anterior HoxB genes by RARs, among other examples. Altogether, our findings identify genome-wide targets of RA signaling during embryonic development and provide a molecular mechanism by which developmental signaling pathways regulate the expression of target genes by altering chromatin topology.
2023-06-13 | GSE233695 | GEO
Project description:Retinoic acid (RA) functions as a ligand for the nuclear RA receptors (RARs), which regulate the expression of target genes by binding to RA response elements. RA signaling is required for multiple processes during chordate embryonic development, such as body axis extension, hindbrain antero-posterior patterning and forelimb bud initiation. Although some RA target genes have been identified, little is known about the genome-wide effects of RA signaling during in vivo embryonic development. Here we stimulate the RA pathway during development by treating zebrafish embryos with all-trans-RA (atRA), the most abundant form of RA, and use a combination of RNA-seq, ATAC-seq, ChIP-seq and HiChIP to gain insight into the molecular mechanisms by which RA signaling control target gene expression. We find that RA signaling is involved in anterior/posterior patterning and development of the central nervous system, participating in the transition from pluripotency to differentiation. atRA treatment also induces alterations in chromatin accessibility during early development and promotes chromatin binding of RARaa and the RA targets Hoxb1b, Meis2b and Sox3, which cooperate in central nervous system development. Finally, we show that RA induces a rewiring of chromatin architecture, with alterations in chromatin 3D interactions that are consistent with target gene expression. This is illustrated by the specific induction of anterior HoxB genes by RARs, among other examples. Altogether, our findings identify genome-wide targets of RA signaling during embryonic development and provide a molecular mechanism by which developmental signaling pathways regulate the expression of target genes by altering chromatin topology.
2023-06-13 | GSE233691 | GEO