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

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

PROVIDER: PRJNA1150249 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30316140_1.fastq.gz	Fastqsanger.gz
	SRR30316140_2.fastq.gz	Fastqsanger.gz
	SRR30316141_1.fastq.gz	Fastqsanger.gz
	SRR30316141_2.fastq.gz	Fastqsanger.gz
	SRR30316142_1.fastq.gz	Fastqsanger.gz

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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

The identification of genes altered by RORα in progression of non-alcoholic steatohepatitis (NASH)

Project description:Purpose: To identify the target genes of RORα associated with development of NASH Methods: RNA isolation for sequencing analysis from liver tissues of High fat diet (HFD)-fed RORα-LKO and RORα f/f mice and mRNA-sequencing Conclusion: When calcuated by dividing the normalized read count of HFD-fed RORα-LKO by that of RORαf/f,.there are 8505 genes altered by RORα deletion (cut-off, 0.8-fold, 1.5-fold).

2019-12-03 | GSE90844 | GEO

RORɣt and RORα Signature Genes in Human Th17 Cells

Project description:In an effort to study gene expression modulated by RORɣt and RORα in human Th17 cells, global gene expression of human CD4 T cells activated under Th17 skewing conditions was profiled by RNA sequencing. RORɣt and RORα signature genes were identified in these Th17 cells treated with specific siRNAs to knock down RORɣt or RORα expression. In addition, selective small molecule RORɣt modulators were also utilized as pharmacological tools in RORɣt signature gene identification.

2017-09-14 | GSE103844 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [ChIP-seq]

Project description:Inflammatory bowel disease (IBD) is multi-factorial chronic intestinal inflammation driven by pathogenic T cells. The mechanisms underlying colitis pathogenicity and anti-TNF therapy resistance are not fully understood. Here we demonstrate that RORα is highly expressed in active UC patients, particularly in those non-responsive to anti-TNF treatment. Rorα deficient CD4+ T cells could not induce severe gut inflammation in a T cell transfer colitis model. Mechanistically, RORα regulated T cell infiltration in colon by promoting T cell migration and inhibiting T cell apoptosis. Meanwhile, genome-wide occupancy and transcriptome analysis revealed that RORα promoted mTORC1 activation. mTORC1 signaling, also hyperactivated in active UC patients, was necessary for T cell-mediated colitis.

2021-07-28 | GSE168217 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [RNA-seq]

2021-07-28 | GSE168216 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [16S rRNA-seq]

2021-07-28 | GSE168218 | GEO

Inhibition of nuclear receptor RORα attenuates cartilage damage in osteoarthritis by modulating IL-6/STAT3 pathwa

Project description:Osteoarthritis is characterized by cartilage destruction, chronic inflammation, and subchondral sclerosis. Evidence showed that nuclear receptor family is closely associated with cartilage damage in an unclear molecular mechanism. Here, we investigated the role and molecular mechanism of the retinoic acid receptor-related orphan receptor-α (RORα), an important member of nuclear receptor, in regulating cartilage degradation and osteoarthritis pathogenesis. Investigation to osteoarthritis clinical specimen showed that the degree of RORα elevation is positively correlated with the severity of osteoarthritis and cartilage damage. In an in vivo osteoarthritis models induced by anterior crucial ligament transaction, intraarticularly injection of siRora adenovirus reversed the cartilage damage. RORα knock-down increased the protein expression level of anabolic factor such as type II collagen, Aggrecan, and decreased the expression of catabolic factor. RNA-seq data suggested IL-6/STAT3 pathway is significantly down-regulated. Mechanistically, RORα knock-down decreased the expression level of both IL-6 and phosphorylated STAT3. RORα exerted its effect on IL-6/STAT3 signaling in two different ways, which includes interaction with STAT3 and IL6 promoter. Taken together, our findings indicated the pivotal role of RORα/IL-6/STAT3 axis in osteoarthritis progression and confirmed RORα knock-down exerted therapeutic effect in human chondrocyte thus providing a potential drug target in osteoarthritis therapy.

2021-04-20 | GSE172291 | GEO

Transcriptomic evaluation of skin tape-strips in children with allergic asthma uncovers epidermal barrier dysfunction and asthma-associated biomarkers abnormalities

Project description:Tape-strips were obtained from skin of 18 pediatric patients with moderate allergic asthma (MAA) (n=11), severe allergic asthma (SAA) (n=9), and from healthy children (n=12) and analyzed with bulk RNA-sequencing (RNA-seq). Differential expression was defined as |fold change|≥2 and false discovery rate<0.05. MAA and SAA shared downregulation of G-protein-coupled receptor- (GPCR), mitochondria-, and Wnt-signaling-related genes. Terminal differentiation (FLG/filaggrin), cell adhesion (CDH19, JAM2), lipid biosynthesis/metabolism (ACOT2, LOXL2) markers were significantly downregulated in MAA and SAA (FDR<0.05). Many of these markers additionally correlated with metrics of asthma severity (e.g. exacerbation rate per year, forced expiratory volume in 1 second [FEV1] [% predicted], impulse oscillometry [IOS] R5-20 Hz, fractional excretion of nitric oxide [FeNO]).

2024-07-25 | GSE245608 | GEO

Gut-derived short-chain fatty acids modulate skin barrier integrity by promoting keratinocyte metabolism and differentiation

Project description:Barrier integrity is central to the maintenance of a healthy immunological homeostasis. Impaired skin barrier function is linked with enhanced allergen sensitization and the development of diseases such as atopic dermatitis (AD), which can precede the development of other allergic diseases such as food allergies and asthma. Epidemiological evidence indicates that children suffering from allergies have lower levels of dietary fibre-derived short-chain fatty acids (SCFA). Using an experimental model of AD, we report that a fermentable fibre-rich diet alleviates AD severity and systemic allergen sensitization. The gut-skin axis underpins this phenomenon through SCFA, which strengthen skin barrier integrity by altering mitochondrial metabolism of epidermal keratinocytes. SCFA promote keratinocyte differentiation and the production of key structural lipids, resulting in enhanced barrier function. Our results demonstrate that dietary fibre and SCFA mitigate AD by improving barrier integrity, ultimately limiting early systemic allergen sensitization and development of disease.

2022-08-24 | GSE185640 | GEO

RORα coordinates thalamic and cortical maturation to instruct barrel cortex development.

Project description:The retinoic acid orphan receptor alpha (RORα) is well known for its role in cerebellar development and maturation as revealed in the stagerrer (Stg) mutant mouse line. However it’s potential involvement for the development of other brain regions has not been assessed. Here we describe a new role of RORα in the development of the thalamic and cortical circuits that leads to the assembly of columnar barrel structures in the primary somatosensory cortex. Microarray analyses comparing gene expression in the thalamus and cortex of the Stg, showed a down-regulation of genes that have been involved in the control of TCA or cellular maturation of layer IV neurons. Overall, our study outlines a new role of RORα for the coordinated maturation of the thalamus and cortex during early postnatal life, and shows that it is required to initiate the transcription of genes involved in barrel formation.

2017-09-30 | GSE80317 | GEO

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