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Expression analysis of epidermal barrier functions associated genes in mouse epidermis treated by All-trans retinoic acid and Nicotinamide

ABSTRACT: Investigation of molecular mechanisms of impaired skin barrier by ATRA in mouse epidermis

ORGANISM(S): Mus musculus

PROVIDER: GSE124181 | GEO | 2018/12/21

REPOSITORIES: GEO

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Expression analysis of epidermal barrier functions associated genes in HaCaT cell treated by All-trans retinoic acid and Nicotinamide

Project description:Investigation of molecular mechanisms of impaired skin barrier by ATRA

2018-12-21 | GSE124179 | GEO

Expression analysis of epidermal barrier functions associated genes in mouse epidermis treated by All-trans retinoic acid and Nicotinamide

Project description:Expression analysis of epidermal barrier functions associated genes in mouse epidermis treated by All-trans retinoic acid and Nicotinamide

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Expression analysis of epidermal barrier functions associated genes in HaCaT cell and mouse epidermis treated by All-trans retinoic acid and Nicotinamide

Project description:Expression analysis of epidermal barrier functions associated genes in HaCaT cell and mouse epidermis treated by All-trans retinoic acid and Nicotinamide

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Expression analysis of epidermal barrier functions associated genes in HaCaT cell and mouse epidermis treated by All-trans retinoic acid and Nicotinamide

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-12-21 | GSE124183 | GEO

The retinoid X receptor has a critical role in synthetic rexinoid-induced increase in cellular all-trans-retinoic acid

Project description:Rexinoids are agonists of nuclear rexinoid X receptors (RXR) that heterodimerize with other nuclear receptors to regulate gene transcription. A number of selective RXR agonists have been developed for clinical use but their application has been hampered by the unwanted side effects associated with the use of rexinoids and a limited understanding of their mechanisms of action across different cell types. Our previous studies showed that treatment of organotypic human epidermis with the low toxicity UAB30 and UAB110 rexinoids resulted in increased steady-state levels of all-trans-retinoic acid (ATRA), the obligatory ligand of the RXR-RAR heterodimers. Here, we investigated the molecular mechanism underlying the increase in ATRA levels using a dominant negative RXRα that lacks the activation function 2 (AF-2) domain. The results demonstrated that overexpression of dnRXRα in human organotypic epidermis markedly reduced signaling by resident ATRA, suggesting the existence of endogenous RXR ligand, diminished the biological effects of UAB30 and UAB110 on epidermis morphology and gene expression, and nearly abolished the rexinoid-induced increase in ATRA levels. Global transcriptome analysis of dnRXRα-rafts in comparison to empty vector-transduced rafts showed that over 95% of the differentially expressed genes in rexinoid-treated rafts constitute direct or indirect ATRA-regulated genes. Thus, the biological effects of UAB30 and UAB110 are mediated through the AF-2 domain of RXRα with minimal side effects in human epidermis. As ATRA levels are known to be reduced in certain epithelial pathologies, treatment with UAB30 and UAB110 may represent a promising therapy for normalizing the endogenous ATRA concentration and signaling in epithelial tissues.

2024-04-02 | GSE244387 | GEO

Expression analysis of epidermal barrier functions associated genes in HaCaT cell treated by All-trans retinoic acid and Nicotinamide

Project description:Expression analysis of epidermal barrier functions associated genes in HaCaT cell treated by All-trans retinoic acid and Nicotinamide

| PRJNA510952 | ENA

All‑trans retinoic acid alters the expression of the tight junction proteins Claudin‑1 and ‑4 and epidermal barrier function‑associated genes in the epidermis.

Project description:All‑trans retinoic acid (ATRA) regulates skin cell proliferation and differentiation. ATRA is widely used in the treatment of skin diseases, but results in irritation, dryness and peeling, possibly due to an impaired skin barrier, although the exact mechanisms are unclear. The present study established an ATRA‑associated dermatitis mouse model (n=32) in order to examine the molecular mechanisms of skin barrier impairment by ATRA. Changes in epidermal morphology and structure were observed using histological examination and transmission electron microscopy (TEM). Gene expression was analyzed by microarray chip assay. Histology and TEM demonstrated pronounced epidermal hyperproliferation and parakeratosis upon ATRA application. The stratum corneum layer displayed abnormal lipid droplets and cell‑cell junctions, suggesting alterations in lipid metabolism and dysfunctional cell junctions. Gene expression profiling revealed that factors associated with epidermal barrier function were differentially expressed by ATRA, including those associated with tight junctions (TJs), cornified envelopes, lipids, proteases, protease inhibitors and transcription factors. In the mouse epidermis, Claudin‑1 and ‑4 are proteins involved in TJs and have key roles in epidermal barrier function. ATRA reduced the expression and altered the localization of Claudin‑1 in HaCaT immortalized keratinocytes and the mouse epidermis, which likely leads to the disruption of the epidermal barrier. By contrast, Claudin‑4 was upregulated in HaCaT cells and the mouse epidermis following treatment with ATRA. In conclusion, ATRA exerts a dual effect on epidermal barrier genes: It downregulates the expression of Claudin‑1 and upregulates the expression of Claudin‑4. Claudin‑4 upregulation may be a compensatory response for the disrupted barrier function caused by Claudin‑1 downregulation.

| S-EPMC6414175 | biostudies-literature

Epidermal RORα maintains barrier integrity and prevents allergic inflammation by regulating late differentiation and lipid metabolism

Project description:The skin epidermis provides a vital barrier for preventing transepidermal water loss (TEWL) and environmental stimuli. However, the molecular mechanisms ensuring barrier integrity remain not fully understood. RORα is a nuclear receptor highly expressed in the epidermis of normal skin. However, its epidermal expression is significantly reduced in the lesions of multiple inflammatory skin diseases. In this study, using mice with epidermis-specific Rora gene deletion (RoraEKO), we have demonstrated the central roles of RORα in stabilizing skin barrier function. Albeit the lack of spontaneous skin lesion or dermatitis, RoraEKO mice exhibited elevated TEWL rate and skin features indicating barrier dysfunction. The histological and lipidomic analysis uncovered low levels of cornified envelope proteins and aberrant ceramide composition in the RoraEKO epidermis, implying disturbed late epidermal differentiation. In parallel, RNA-seq analysis revealed altered transcription levels of gene clusters related to “keratinization” and “lipid metabolism” in RORα deficient epidermis. Importantly, epidermal Rora ablation greatly amplified percutaneous allergic inflammatory responses to oxazolone in a mouse allergic contact dermatitis (ACD) model. Our results substantiated the essence of epidermal RORα in maintaining late keratinocyte differentiation and normal barrier function while suppressing cutaneous inflammation.

2024-10-23 | GSE275323 | GEO

Clinical Trial of All-trans-retinoic Acid, Bevacizumab and Atezolizumab in Colorectal Cancer

Project description:The main purpose of this clinical trial is to learn about the good and the bad effects of all trans retinoic acid (ATRA), atezolizumab and bevacizumab as a possible treatment for advanced colorectal patients. Participants will be treated with the following combination of these drugs: 1. ATRA will be given in a pill form to be taken twice a day at home for 7 days starting on day 1 of a cycle. 2. Atezolizumab will be given through a vein in arm or through mediport over 60-90 minutes every 2 weeks in the outpatient chemotherapy infusion centers at UTSW. 3. Bevacizumab will be given through a vein in arm or through mediport over 20-40 minutes every 2 weeks in the outpatient chemotherapy infusion centers at UTSW.

| 70824 | ecrin-mdr-crc

Grhl3 is essential for epidermal barrier repair from both physical and immune injury, relevance to lesional skin disease

Project description:Epidermal barrier repair mechanisms activated in psoriasis lesions are likely involved in limiting the severity of this disease. We show that loss of grainyhead-like 3 (Grhl3), a pro-terminal differentiation factor in the epidermis, is sufficient to trigger greater sensitivity to and delayed resolution of epidermal lesions resulting from either physical or immune mediated barrier injury. After stimulation of Toll like receptors, the loss of Grhl3 resulted in increased epidermal damage with a striking increase in basal cell proliferation, hyperplasia of partially differentiated suprabasal layers, and a transcriptional profile highlighted by the overexpression of epidermal wound response and alarmin genes. This study reveals an important role for the epidermis in the initiation and recovery from immune-mediated lesions, and indicated that the epidermal regulator Grhl3 acts to both suppress disease initiation and resolve existing lesions. This work suggests that treatments focused on improving barrier function could be used preventatively and therapeutically in psoriasis. Whole skin was collected from E16.5 mouse backskins for Grhl3 ChIP. Adult epidermis for depilation and imiquimod experiments was seperated from dermis using dispase prior to Grhl3 ChIP.

2014-09-01 | E-GEOD-52648 | biostudies-arrayexpress

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