Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of human sebocytes (SEB-1) treated with 13-cis retinoic acid treatment

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Diane Thiboutot

PROVIDER: E-GEOD-10432 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Neutrophil gelatinase-associated lipocalin mediates 13-cis retinoic acid-induced apoptosis of human sebaceous gland cells.

Nelson Amanda M AM Zhao Wei W Gilliland Kathryn L KL Zaenglein Andrea L AL Liu Wenlei W Thiboutot Diane M DM

The Journal of clinical investigation 20080401 4

13-cis retinoic acid (13-cis RA; also known as isotretinoin) is the most potent agent available for treatment of acne. It is known that the drug induces apoptosis in cells cultured from human sebaceous glands, but its mechanism of action has not been determined. In this study, skin biopsies were taken from 7 patients with acne prior to and at 1 week of treatment with 13-cis RA. TUNEL staining confirmed that 13-cis RA induced apoptosis in sebaceous glands. Transcriptional profiling of patient ski ...[more]

PMID: 18317594

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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

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. 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. This SuperSeries is composed of the SubSeries listed below.

Project description:Staphylococcus Enterotoxin B (SEB) is an exotoxin produced by Staphylococcus aureus. It is a public health threat during nosocomial infections. It is also considered as a biological weapon. The Centers for Disease Control and Prevention (CDC) lists SEB as a category B agent of Biodefence. SEB is easily aerosolized and can enter the host through inhalation which could lead to Acute Lung Injury (ALI) and in severe cases, it may result in multiple organ failure, shock and death. It is considered to be a Super-antigen as it activates a large number (30%) of T cells and results in the production of cytokines SEB binds directly to the non polymorphic region of MHC Class II which is expressed on antigen presenting cells and this complex activates T cells expressing a specific variable region of the β chain (Vβ8) of the T cell receptor (TCR). Thus, inhalation of SEB leads to recruitment of immune cells into the lung and secretion of pro-inflammatory cytokines which results in severe damage to the lung by increasing the permeability, and induction of respiratory failure. MicroRNA (miRNAs) is considered one of the mechanisms by which the epigenetic regulation happens. MicroRNA are noncoding small RNAs that have recently been shown to play a role in gene expression. The action of miRNA is dependent on its binding to 3’ Untranslated Region (3’UTR) of mRNA resulting in transcriptional or translational repression. Specifically, the efficacy of gene silencing is determined by the interaction of miRNA seed sequence with the target mRNA. Endocannabinoids are lipid molecules produced endogenously by host cells and bind to cannabinoid receptors, CB1 and CB2. N-Arachidonoylethanolamide or anandamide (AEA) is an endocannabinoid that has been shown to have immunomodulatory effects by our lab and others, although the precise mechanism is not clear. So far through my research, I found that Endocannabinoid is involved in a very unique way in the anti-inflammatory response through upregulation of many anti-inflammatory genes such as FOXP3, ARG1, and IL-10 that targeted by miRNA23a-3p and miRNA 34a-5p as well as the anti-inflammatory phenotype population as it show in the RT-PCR and flow cytometry results.

Dataset Information

Transcription profiling of human sebocytes (SEB-1) treated with 13-cis retinoic acid treatment

Publications

Neutrophil gelatinase-associated lipocalin mediates 13-cis retinoic acid-induced apoptosis of human sebaceous gland cells.

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