Rheumatoid arthritis (RA) is a systemic autoimmune disease and its underlying molecular mechanisms are still poorly understood. Previously a CD4 T-cell microarray study has only focused arthritis patients. We aimed to compare the molecular profiles of active RA versus healthy control in CD4 T cells.
CD4 T-cell transcriptome analysis reveals aberrant regulation of STAT3 and Wnt signaling pathways in rheumatoid arthritis: evidence from a case-control study.
Specimen part, Disease, Disease stage
View SamplesWe reported the whole transcriptome resequencing in rattus adipose-derived mesenchymal stem cells and BMP-2 induced cels, including mRNA, lincRNA and circRNA
No associated publication
Sex, Specimen part, Cell line
View SamplesC1q expression increases significantly in the peripheral blood of patients with active tuberculosis compared to healthy controls and individuals with latent TB infection. The percentage of C1q-expressing CD14 positive cells is significantly increased in active TB patients. C1q expression in the peripheral blood correlates with sputum smear positivity in tuberculosis patients and is reduced after anti-tuberculosis chemotherapy. Notably, receiver operating characteristic analysis showed that C1qC mRNA levels in peripheral blood efficiently discriminate active from latent tuberculosis infection and healthy controls. Additionally, C1qC protein level in pleural effusion shows improved power in discriminating tuberculosis from non-tuberculosis pleurisy when compared to other inflammatory markers, such as IL-6 and TNF-
Increased complement C1q level marks active disease in human tuberculosis.
Specimen part, Disease, Disease stage
View SamplesEmerging evidence suggests that microRNAs (miRNAs) are crucially involved in tumorigenesis and that paired expression profiles of miRNAs and mRNAs can be used to identify functional miRNA-target relationships with high precision.However, no studies have applied integrated analysis to miRNA and mRNA profiles in chordomas.
No associated publication
Sex, Age, Specimen part
View SamplesAnalysis of ejaculated spermatozoav from normozoospermic men and asthenozoospermic men. Some of genes were up-regulated or down-regulated in asthenozoospermia, and their abnormal expression were the causes of the impaired sperm motility. Results provide insight into the mechanisms by which asthenozoospermia is controlled.
Functional expression of ropporin in human testis and ejaculated spermatozoa.
Specimen part
View SamplesIn proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PCR2 writing of H3K27me3 is mechanistically required for gene silencing. Here we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (Embryonic Ectoderm Development) inactivation in the postnatal heart (Eed CKO ) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in Eed CKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized Eed CKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.
EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A systematic analysis of the skeletal muscle miRNA transcriptome of chicken varieties with divergent skeletal muscle growth identifies novel miRNAs and differentially expressed miRNAs.
Specimen part
View SamplesThe genetic closeness and divergent muscle growth rates of broilers and layers make them great models for myogenesis study. In order to discover the molecular mechanisms determining the divergent muscle growth rates and muscle fiber sizes in different chicken lines, we systematically identified differentially expressed genes between broilers and layers during muscle development (embyonic day 10, 12, 14 and 18) by microarray hybridization experiment.
A systematic analysis of the skeletal muscle miRNA transcriptome of chicken varieties with divergent skeletal muscle growth identifies novel miRNAs and differentially expressed miRNAs.
Specimen part
View SamplesThe molecular explanation for tamoxifen serving as a breast cancer treatment but displaying partial estrogenic in the uterus is not known. Previously, we reported that differential promoter context and cofactor recruitment contribute to the tissue specificity of tamoxifen. Here, we investigated the genomic basis for the partial oestrogenic activity of tamoxifen in the endometrium. We showed that tamoxifen not only affects the rate of transcription of oestrogen target genes but also targets a unique set of genes. Since oestrogen and tamoxifen are both able to bind to oestrogen receptors (ERs) and because both promote endometrial carcinogenesis, we hypothesized that the molecular effectors for ERs in endometrial carcinogenesis most likely reside in genes that are commonly targeted by oestrogen and tamoxifen. Among those target genes, we identified a paired-box gene PAX2 that is critically involved in cell proliferation and carcinogenesis in the endometrium. Our experiments also demonstrated that PAX2 is activated by oestrogen and tamoxifen in endometrial carcinomas but not in normal endometrium, and this activation is associated with cancer-linked hypomethylation of the PAX2 promoter.
Hypomethylation-linked activation of PAX2 mediates tamoxifen-stimulated endometrial carcinogenesis.
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View SamplesThrough H3K27me3 and H3K27ac ChIP-seq and microarray data in wile-tpye (WT) and EED-knockout (CKO) mouse cardiomyocytes, we unexpectedly uncovered a novel mechanism of PRC2-mediated gene repression. EED inactivation in the postnatal heart (EEDCKO) caused progressive, lethal dilated cardiomyopathy, with upregulation of components of the slow-twitch muscle gene program. Surprisingly, upregulation of these genes was not associated with their loss of H3K27me3, but rather with their gain of H3K27 acetylation (H3K27ac), an activating histone mark4,5. Moreover, re-expression of EED in juvenile hearts rescued heart function and normalized H3K27ac, but not H3K27me3.
No associated publication
Specimen part
View Samples