JAK inhibitors like tofacitinib were thought to act primarily on T cells. However, our data and recent research suggest that JAK receptors are also present on keratinocytes. Here, we show effect of tofacitinib on primary keratinocytes, which could explain effects of topical tofacitinib treatment in psoriasis.
Tofacitinib Represses the Janus Kinase-Signal Transducer and Activators of Transcription Signalling Pathway in Keratinocytes.
Specimen part
View SamplesmiR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara).
MicroRNA-146a suppresses IL-17-mediated skin inflammation and is genetically associated with psoriasis.
Age, Specimen part
View SamplesMiR-31 is one of the most highly overexpressed miRNAs in psoriasis skin; however, its biological role in the disease has not been studied. Here we show that miR-31 is markedly overexpressed in psoriasis keratinocytes. To study the biological role of miR-31 in keratinocytes, we transfected miR-31 hairpin inhibitor (anti-miR-31) into primary human keratinocytes to inhibit endogenous miR-31. We performed a global transcriptome analysis of keratinocytes upon suppression of endogenous miR-31 using Affymetrix arrays.
MicroRNA-31 is overexpressed in psoriasis and modulates inflammatory cytokine and chemokine production in keratinocytes via targeting serine/threonine kinase 40.
Specimen part
View SamplesThe lncRNA LOC100130476 (named as WAKMAR2) was found to be down-regulated in epidermal keratinocytes in human chronic non-healing wounds compared to normal acute wounds and the intact skin. However, its biological role in keratinocytes during wound repair has not been studied.
WAKMAR2, a Long Noncoding RNA Downregulated in Human Chronic Wounds, Modulates Keratinocyte Motility and Production of Inflammatory Chemokines.
Specimen part
View SamplesWe report the transcriptome analysis of epidermal CD8 tissue resident memory T (TRM) cells from healthy human skin. Specifically, epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells from healthy human skin were sorted by FACS. Differential gene expression analysis revealed functional dichotomy of epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells. Overall design: Analysis of differentially expressed genes between epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- T cells from healthy human skin, biological replicates (n=7) (healthy skin donors).
CD49a Expression Defines Tissue-Resident CD8<sup>+</sup> T Cells Poised for Cytotoxic Function in Human Skin.
Specimen part, Subject
View SamplesCholestasis may cause cholemic nephropathy that can be modelled in common bile duct ligated (CBDL) mice. We aimed to explore the therapeutic efficacy and mechanisms of norursodeoxycholic acid (norUDCA) in cholemic nephropathy. To determine whether norUrsodeoxycholic acid (norUDCA) prevents cholemic nephropathy in long-term CBDL mice, a norUDCA-enriched diet (0.125% w/v, corresponding to 200 mg/kg/day for a mouse of 25 g body weight eating about 4g daily) or a standard mouse diet (Sniff, Soest, Germany) were started 5 days prior to CBDL and were continued until harvesting 3 weeks thereafter. For transcriptional profiling using microarray technology, we compared sham-operated (SOP) mice and 3-week CBDL mice that were either fed 0.125% norUDCA-enriched or standard mouse diets.
NorUrsodeoxycholic acid ameliorates cholemic nephropathy in bile duct ligated mice.
Specimen part
View SamplesExpression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours.
The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.
Cell line
View SamplesMice wild type or knocked-out for the MyD88 gene specifically in liver, were recruited for this expression profiling experiment. Each group of mice (WT versus LKO) were fed with a control diet or a high fat diet. Then mice were sacrificed and liver samples form were processed for RNA extraction. Total liver RNA of each sample was then pooled with those of the same group and treatment for microarray hybridization.
Hepatocyte MyD88 affects bile acids, gut microbiota and metabolome contributing to regulate glucose and lipid metabolism.
Age, Specimen part
View SamplesIt has been unclear whether ischemic stroke induces neurogenesis or neuronal DNA-rearrangements in the human neocortex. We show here that neither is the case, using immunohistochemistry, transcriptome-, genome- and ploidy-analyses, and determination of nuclear bomb test-derived 14C-concentration in neuronal DNA. A large proportion of cortical neurons display DNA-fragmentation and DNA-repair short time after stroke, whereas neurons at chronic stages after stroke show DNA-integrity, demonstrating the relevance of an intact genome for survival. Overall design: Analyze of potential fusion transcripts in 13 samples, seven cortical ischemic stroke tissue and six control cortex, by deep sequencing using Illumina HiSeq 2000
The age and genomic integrity of neurons after cortical stroke in humans.
No sample metadata fields
View SamplesMultiple Endocrine Neoplasia Tumor Syndrome type 1 (MEN 1) is an autosomal dominant tumor syndrome affecting individuals with a heterozygous germline mutaion of the MEN1 gene. MEN 1 carriers commonly develop parathyroid, anterior pituitary, duodenal and pancreatic endocrine tumors. The phenotype of existing mouse models for the MEN 1 syndrome, with a germline heterozygous (hz) Men1 gene inactivation, show close resemblance to the human MEN 1 syndrome. Menin, the protein encoded for by the MEN1/Men1 gene, lacks homology with known proteins, and evidence of its involvement in different cellular processes is steadily growing. Several interaction partners have been identified, involving different interaction sites on the menin protein. Accumulating evidence suggests a role for menin in transcriptional regulation, cell cycle control, apoptosis, chromatin modification and DNA damage response and repair. Loss of heterozygosity (LOH) of the MEN1 gene precedes tumor formation in the MEN 1 heterozygous pancreas. We set out to determine if there is a change in gene expression early on in the hz islet, as compared with islets in wildtype (wt) littermates, long before the LOH events occur. We performed a global mRNA expression microarray on islets from young, five-week-old, hz Men1 mice and their wt littermates, and we have subsequently corroborated a subset of the findings on the qPCR and protein level.
Accelerated proliferation and differential global gene expression in pancreatic islets of five-week-old heterozygous Men1 mice: Men1 is a haploinsufficient suppressor.
Sex, Age, Specimen part
View Samples