To search for biomarkers to differentiate Adult-Onset Steroid Sensitive focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD).
Comparison of Glomerular Transcriptome Profiles of Adult-Onset Steroid Sensitive Focal Segmental Glomerulosclerosis and Minimal Change Disease.
Specimen part, Disease, Disease stage
View SamplesLiver fibrosis is a high-morbidity and high-mortality chronic disease throughout the world without any satisfying treatment Large-conductance Ca2+- and voltage-activated K+ (Slo1, BK) channels are widely expressed in human body and important for numerous physiological processes. Previous studies have shown that BK channels are expressed in HSCs of patients with liver fibrosis and they are involved in contraction/relaxation of the HSCs To investigate the molecular mechanism of antifibrotic effect of BK channel opener rottlerin using in vivo fibrosis models. transcriptomic analyses of differential expression genes in livers from rats of vehicle, CCl4 and CCl4 combined with rottlerin treatment were for discrimination. The RNA samples were extracted from three samples of each group for microarray profiling and performed in Affymetrix Rats Genome 230 2.0 arrays for gene expression profiling analysis, which contained 31 042 probe sets. The biotinylated cRNA targets were hybridized with the microarray. After hybridization, arrays were stained in the Fluidics Station 450 and scanned on the Affymetrix Scanner 3000. The microarray experiments were performed by following the protocol of Affymetrix Inc at Shanghai Biotechnology Corporation. Under the criteria fold change > 1.5 or < 0.67, we obtained 10672 differential expressed genes (DEGs) between CCl4 and CCl4 combined with rottlerin treatment group, and the data was applied to further analysis.
Activation of BK Channels Prevents Hepatic Stellate Cell Activation and Liver Fibrosis Through the Suppression of TGFβ1/SMAD3 and JAK/STAT3 Profibrotic Signaling Pathways.
Specimen part
View SamplesThe serine threonine kinase Stk40 has been shown to involve in mouse embryonic stem cell differentiation, pulmonary maturation and adipocyte differentiation. Here we report that targeted deletion of Stk40 leads to fetal liver hypoplasia and anemia in the mouse embryos. The reduction of erythrocytes in the fetal liver is accompanied by increased apoptosis and compromised erythroid maturation. Stk40-/- fetal liver cells have significantly reduced colony forming units (CFUs) capable of erythroid differentiation, including burst forming unit-erythroid (BFU-E), colony forming unit-erythroid (CFU-E), and CFU-granulocyte, erythrocyte, megakaryocyte and macrophage (CFU-GEMM), but not CFU-granulocyte/macrophages (CFU-GM). Purified Stk40-/- megakaryocyte-erythrocyte progenitors (MEPs) produced substantially fewer CFU-E colonies compared to control cells. Moreover, Stk40-/- fetal liver erythroblasts failed to form normal erythroblastic islands in association with wild type or Stk40-/- macrophages, indicating an intrinsic defect of Stk40-/- erythroblasts. Furthermore, the hematopoietic stem and progenitor cell pool is reduced in Stk40-/- fetal livers but still retains the multi-lineage reconstitution capacity. Finally, analysis of microarray data of E14.5 fetal liver cells suggests a potential role of aberrantly activated TNF- signaling in Stk40 depletion induced dyserythropoiesis with a concomitant increase in cleaved Caspase-3 and decrease in Gata1 proteins. Altogether, the identification of Stk40 as a regulator for fetal erythroid differentiation, maturation and survival provides new clues to the molecular regulation of erythropoiesis and related diseases.
Deletion of Stk40 impairs definitive erythropoiesis in the mouse fetal liver.
Specimen part
View SamplesCollagen triple helix repeat containing 1 (CTHRC1) has been found to be up-regulated in many human solid tumors. In this study, we investigated the changes of gene expression by comparing CTHRC1-siRNA and Scramble-siRNA control in hepatocellular carcinoma cell line HCCLM3, which has high expression levels of CTHRC1.
No associated publication
Cell line
View SamplesMutations of SMAD family member 4 (Smad4) gene caused Hereditary Hemorrhagic Telangiectasia (HHT). It was believed that bleeding disorders were caused by arteriovenous malformation in this syndrome. Although several studies indicated dysfunction of platelets from HHT patient, the role(s) of smad4 in platelet function has not been examined. In this study, using megakaryocyte/platelet-specific Smad4-deficient mice, we investigated the physiological function of Smad4 in platelet activation and the underlying mechanism.
No associated publication
Specimen part
View SamplesWe used microarrays to detail the global programme of gene expression underlying the coculturing of degenerate NPCs and ASCs and identified distinct classes of altered genes and ncRNAs during this process.
Aberrantly expressed messenger RNAs and long noncoding RNAs in degenerative nucleus pulposus cells co-cultured with adipose-derived mesenchymal stem cells.
Specimen part
View SamplesThe renewing human epidermis constantly senses and adapts to a wide range of mechanical cues that are ubiquitous throughout life. The mechanisms of how mechanical forces are responded by interfollicular epidermal stem cells (IFESCs) and are transmitted directly into nucleus to modify gene expression remain incompletely defined. In vitro, human IFESCs were cultured on the collagen I coated silicon rubber membrane and then subjected to the mechanical stretched. Cyclic mechanical tension at 0.5 Hz sinusoidal curve at 10% elongation was applied using an FX-5000T Flexercell Tension Plus unit (Flexcell International Corporation). In mechanical unloading groups, cells were cultured on the same plates in the same incubator with the mechanical stretched groups but not subjected to stretch. Combining genome-wide microarray and functional analyses, we made transcriptome analysis of samples from the mechanical unstretched or stretched isolated human IFESCs.
No associated publication
Specimen part, Treatment
View SamplesHepatitis B virus (HBV) infection is a leading risk factor for liver fibrosis (LF) and hepatocellular carcinoma. Emerging evidence indicates that host genetic, virological and immunological factors will influence the fibrotic progress. Many previous studies have focused on specific pathways or genes included in LF mechanism, however global view of the whole genome expresion profile in HBV related LF patients never been studied, and the mechanisms underlying the promotion of liver fibrosis progression remain obscure. Here we collected liver biopsy samples from 124 chronic hepatitis B (CHB) patients and used Affymetrix HG U133 Plus 2.0 microarray to quantify the transcriptome of these patients. Through integrated data analysis, including geneset enrichment analysis (GSEA), weighted gene co-expression analysis (WGCNA), differential expressed gene (DEG) screening, trend test, principle component analysis (PCA) etc., we identified several key pathways and hub genes participated in the initiation and exacerbation of liver fibrotic progress. The function of these hub genes were also validated by in vitro and in vivo experiments using HepG2, Huh7 and LX-2 cell lines and transgenic mice. This is the first large-scale study investigating the gene expression profile in HBV-related LF patients which will be crucial for unlocking the gene functions and gene-gene correlations in fibrosis progess.
Characterization of gene expression profiles in HBV-related liver fibrosis patients and identification of ITGBL1 as a key regulator of fibrogenesis.
Sex, Age, Specimen part
View SamplesB cells were found to be directly associated with the onset and development of many smoking-induced diseases. However, the in vivo molecular response of B cells underlying the female cigarette smoking remains unknown.
Impact of female cigarette smoking on circulating B cells in vivo: the suppressed ICOSLG, TCF3, and VCAM1 gene functional network may inhibit normal cell function.
Age, Specimen part
View SamplesWhile cold stress has been shown to seriously impact cattle industry, there are only a few reports investigating the effect of cold stress on cattle. Whether severe cold stress results in alterations in gene expression and affects molecular genetic mechanisms remains unknown.
No associated publication
Sex, Specimen part
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