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Profiling of urinary microRNAs in children with atopic dermatitis

ABSTRACT: Atopic dermatitis (AD) is the most prevalent chronic inflammatory skin disease in children characterized by dermatitis and pruritus. MicroRNAs (miRNAs) have been shown as great potential biomarkers for disease fingerprints to predict prognostics. We aimed to identify miRNA signature from serum and urine for the prognosis of AD patient by genome-wide miRNA profiling analysis. Urine from 3 children with AD and 3 healthy children were collected

ORGANISM(S): Homo sapiens

SUBMITTER: Xinghua Gao

PROVIDER: E-GEOD-62403 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Profiling of serum microRNAs in children with atopic dermatitis

Project description:Atopic dermatitis (AD) is the most prevalent chronic inflammatory skin disease in children characterized by dermatitis and pruritus. MicroRNAs (miRNAs) have been shown as great potential biomarkers for disease fingerprints to predict prognostics. We aimed to identify miRNA signature from serum and urine for the prognosis of AD patient by genome-wide miRNA profiling analysis. Serum from 8 children with AD and 8 healthy children were collected

2014-10-17 | E-GEOD-62404 | biostudies-arrayexpress

Profiling of urinary microRNAs in children with atopic dermatitis

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Profiling of serum microRNAs in children with atopic dermatitis

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Profiling of serum and urinary microRNAs in children with atopic dermatitis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-17 | E-GEOD-62406 | biostudies-arrayexpress

EGR1 increases the innervation density of epidermal sensory neurons via upregulation of ARTN in keratinocytes in atopic dermatitis

Project description:Atopic dermatitis (AD) is the chronic inflammatory skin disease accompanied with severe pruritus. To explore the roles of EGR1 in atopic dermatitis and the relationship between EGR1 and pruritus-scratching behavior, we used a atopic dermatitis-like mouse model driven by house dust mite (HDM) treatment in wild type and EGR1 KO mice, followed with RNA-sequencing analysis.

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Establishment of novel atopic dermatitis model by Nestin-cre mediated Ikk2 deficiency

Project description:To generate novel atopic dermatitis model, we used Nestin-cre mediated Ikk2FL/FL mice. Nestincre-mediated conditional knockout mice of Ikk2 gene were generated by crossing female Ikk2FL/FL mice to male Nestin-cre;Ikk2FL/+mice. Nestin-cre;Ikk2FL/FL mice spontaneously develop chronic AD-like skin inflammation and severe pruritus. We further performed Cap analysis of gene expression (CAGE) to elucidate transcriptional profiles in lesional skin of Nestin-cre;Ikk2FL/FL mice.

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Comparing transcriptional profiles of skin biopsies from healthy controls and subjects with chronic pruritus of unknown origin and atopic dermatitis

Project description:Type 2 inflammation contributes to the pathology of pruritic skin diseases such as atopic dermatitis (AD). Chronic pruritus of unknown origin (CPUO) is a skin condition of unknown etiology that typically has minimal inflammation. Yet, some patients with CPUO display signs of mildly increased type 2 inflammation. This study aims to compare skin transcriptional profiles in CPUO to healthy skin and to skin from AD, a classical type 2 inflammatory condition.

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Distinct transcriptomic profiles of early-onset atopic dermatitis in blood and skin of pediatric patients

Project description:Background: Atopic dermatitis (AD) predominantly affects young children, but our understanding of AD pathogenesis is based on skin and blood samples from longstanding adult AD. Genomic biopsy profiling from early pediatric AD showed significant Th2 and Th17/Th22-skewing, without the characteristic adult Th1 up-regulation. Since obtaining pediatric biopsies is difficult, blood gene expression profiling may provide a surrogate for the pediatric skin signature. Objective: To define the blood profile and associated biomarkers of early moderate-to-severe pediatric AD. Methods: We compared microarrays and RT-PCR of blood cells from 28 AD children (<5yrs and within 6 months of disease onset) to healthy control blood cells. Differentially expressed genes/DEGs in blood (fold change/FCH>1.2 and false discovery rate/FDR<0.05) were then compared with skin DEGs. Results: Eosinophil and Th2 markers (IL5RA, IL1RL1/ST2, HRH4, CCR3, SIGLEC8, PRSS33, CLC from gene arrays; IL13/IL4/CCL22 from RT-PCR) were upregulated in early pediatric AD blood, while IFNG/Th1 was decreased. Th1 markers were negatively correlated with clinical severity (EASI, pruritus, transepidermal water loss/TEWL), whereas Th2/Th17-induced IL19 was positively correlated with SCORAD. While a few RT-PCR-defined immune markers (IL13/CCL22) were increased in blood, as previously also reported for skin, there was minimal overlap based on gene array DEGs. Conclusion: The whole blood signature of early moderate-to-severe pediatric AD blood cells show predominantly a Th2/eosinophil profile, but markers largely differ from the skin profile. Given their complementarity, pooling of biomarkers from blood and skin may improve profiling and predictions, providing insight regarding disease course allergic comorbidity development, and response to systemic medications.

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Gene Transcription Abnormalities in Canine Atopic Dermatitis

Project description:Canine atopic dermatitis (AD) is clinically similar to human AD, implicating it as a useful model of human eosinophilic allergic disease. To identify cutaneous gene transcription changes in relatively early inflammation of canine AD, microarrays were used to monitor transcription in normal skin (n=13) and in acute lesional AD (ALAD) and nearby visibly nonlesional AD (NLAD) skin (n=13) from dogs. Scanning the putative abnormally-transcribed genes, several potentially relevant genes, some abnormally transcribed in both NLAD and ALAD (e.g. IL6, NFAM1, MSRA, and SYK), were observed. Comparison for abnormally-transcribed genes common to two related human diseases, human AD and asthmatic chronic rhinosinusitis with nasal polyps (aCRSwNP), further identified genes or gene sets likely relevant to eosinophilic allergic inflammation. These included 1) genes associated with alternatively-activated monocyte-derived cells, including members of the monocyte chemotactic protein (MCP) gene cluster, 2) members of the IL1 family gene cluster, 3) eosinophil-associated seven transmembrane receptor EMR1 and EMR3 genes, 4) interferon-inducible genes, and 5) keratin genes associated with hair and nail formation. Overall, numerous abnormally-transcribed genes were observed only in canine AD; however, many others are common to related human eosinophilic allergic diseases and represent therapeutic targets testable in dogs with AD. Total RNA from skin biopsy specimens from 13 Healthy (i.e. Normal) dogs were compared to total RNA from acute lesional skin biopsy specimens (i.e. ALAD) and nearby visibly nonlesional skin biopsy specimens (i.e. NLAD) from 13 dogs with atopic dermatitis.

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Atopic dermatitis epidermis PCT-DIA

Project description:Atopic Dermatitis (AD) is the most common inflammatory skin disease and characterized by a deficient epidermal barrier and cutaneous inflammation. Genetic studies suggest a key role of keratinocytes in AD pathogenesis, but the alterations in the proteome that occur in the entire epidermis have not been defined. Employing a pressure-cycling technology-data-independent acquisition (PCT-DIA) approach, we performed quantitative proteomics of epidermis from healthy volunteers and lesional and non-lesional skin of AD patients. Results were validated by targeted proteomics using parallel reaction monitoring mass spectrometry or by immunofluorescence staining. The identified proteins reflect the strong inflammation in lesional skin and the defect in keratinocyte differentiation and epidermal stratification. Most importantly, they reveal impaired activation of the NRF2-antioxidant pathway and reduced abundance of mitochondrial proteins involved in key metabolic pathways in the epidermis. These results provide insight into the molecular alterations in the epidermis of AD patients and identify novel targets for pharmaceutical intervention.

2022-10-04 | PXD025431 | Pride

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