Unknown,Transcriptomics,Genomics,Proteomics

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Expression of Autophagy Genes in Myeloproliferative Disorders

ABSTRACT: Comparison of ATG gene family members in MPN pattients with normal controls One-Way ANOVA while contrasting ATG gene family members in 11 Normal (Control) with either 1) 13 PV samples 2) 24 ET samples or 3) 18 PMF samples

ORGANISM(S): Homo sapiens

SUBMITTER: Mike Harr

PROVIDER: E-GEOD-38543 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background: Ameloblast differentiation is the most critical stepwise process in amelogenesis and controlled by a precisely molecules synergistically. To better understand the molecular events defining cell differentiation between preameloblasts and secretory ameloblasts during amelogenesis, a more precise identification of molecules and signaling networks would shed light on the mechanisms governing enamel formation and help lay a foundation for enamel regeneration. Results: Gene expression profiles of human preameloblast and secretory ameloblast cells were obtained using human genome microarrays. From a total of 28,869 analyzed transcripts, 923 differentially expressed genes (DEGs) with FDR<0.01 and Fold-change > 2 were obtained. Among them, more than twice DEGs were found enriched in PAB (n = 647) compared with SAB (n = 276). Notably, 38 genes were identified significantly differentially expressed between PAB and SAB (Fold Change > 8). Comparison of transcriptional profiles of PAB and SAB together with KEGG pathway analysis revealed genes enrichment in PAB were chiefly involved in cell cycle control, DNA damage repair and apoptosis, while genes related to cell adhesion and extracellular matrix had elevated expression level in SAB. Two co-expression modules were further identified significantly associated with the ameloblast differentiation process by weighted gene co-expression network analysis (WGCNA).These gene networks seem to contribute to cell adhesion, tissue development, cell signaling and division. Furthermore, the co-expression associations of RunX2 and BMP8A were also observed in these modules. Conclusions: In this study, we uncovered that the differentiation from PAB to SAB may rely on a highly regulated network of interactions between conserved signal transduction pathways, including members of BMP/TGF-β, Notch, MAPK pathways to coordinate all aspects of ameloblast in intracellular processes and their social contexts. Specifically, expression of genes associated with cell cycle control, DNA damage repair, and apoptosis pathways regulates pre-ameloblast maturation during tooth development. And the SAB cells are regulated by several signaling pathways controlling enamel matrix proteins secretion and cell adhesion, which are critical for enamel formation and cell-cell interactions. Apart from showing the transcriptional patterns of PAB and SAB, the application of bioinformatic analysis also explored the potential key genes and gene-associations in ameloblast differentiation. These findings will aid in the design of new strategies to promote ameloblast functional differentiation in the regeneration and tissue engineering of teeth. Human tooth buds (18-22 weeks) were obtained from fetal cadaver tissue within 3 hours after legal abortion. Teeth were dissected from the mandibles under a laminar flow hood, embedded in OCT compound, and cryosectioned at 10-μm thickness. These sections were used for laser capture microdissection (LCM). In total of 3 pre-ameloblasts and 3 secretory ameloblasts pooled samples were used for RNA extraction and hybridization on Affymetrix microarray.

Project description:We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood. Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at >1.5-fold change and a significant q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in STAT1 and STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, TH1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. This study tested the hypothesis that SpA is characterized by a distinct pattern of gene expression in peripheral blood of affected individuals compared with healthy controls. High-density, human GeneChip probe arrays were used to profile mRNA of peripheral blood cells from 18 subjects with SpA and 25 normal individuals. Samples were processed as two separate sets at different times. Blood samples were taken at a time when patients were not receiving systemic immunomodulatory therapy. Differential expression was defined as a 1.5-fold change with a q value <5%. Gene ontology and pathway information were also studied. Signals from 134 probe sets (representing 95 known and 12 unknown gene transcripts) were consistently different from controls in both Sets 1 and 2. Included among these were transcripts for a group of 20 genes, such as interleukin-1 receptors 1 and 2, NLRP2, SLPI, SPARC, and TREM-1 that are clearly related to the immune or inflammatory response and a group of 4 transcripts that have a strong role in bone remodeling. Our observations are the first to implicate SPARC, SLPI, and NLRP2, a component of the innate immune system, in the pathogenesis of SpA. Our results also indicate a possible role for interleukin-1 and its receptors in SpA. In accord with the bone pathology component of SpA, we also found that expression levels of transcripts reflecting bone remodeling factors are also distinguishable in peripheral blood from patients with SpA versus controls. These results confirm some previously identified biomarkers implicated in the pathogenesis of SpA and also point to novel mediators in this disease. Peripheral blood was collected from diseased and control subjects. The sarcoidosis portion of the study included 12 patients and 12 control subjects. The spondyloarthropathy study was done in two independent sets. The first set included 11 patients and the same 12 control subjects used for the sarcoidosis study. The second set included 7 patients and 13 control subjects. For each sample, total RNA was isolated and analyzed by hybridization on Affymetrix arrays.