Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Genome-wide gene expression profile analysis in pulmonary sarcoidosis

ABSTRACT: We hypothesized that tissue genome-wide gene expression analysis, coupled with gene network analyses of differentially expressed genes, would provide novel insights into the pathogenesis of pulmonary sarcoidosis. Keywords: Disease state analysis Genome-wide gene expression profiles were compared in tissues derived from subjects with active pulmonary sarcoidosis (n=6) and those with normal lung anatomy (n=6). Differentially expressed genes were analyzed by gene network analysis

ORGANISM(S): Homo sapiens

SUBMITTER: Elliott Crouser

PROVIDER: E-GEOD-16538 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gene expression profiling identifies MMP-12 and ADAMDEC1 as potential pathogenic mediators of pulmonary sarcoidosis.

Crouser Elliott D ED Culver Daniel A DA Knox Kenneth S KS Julian Mark W MW Shao Guohong G Abraham Susamma S Liyanarachchi Sandya S Macre Jennifer E JE Wewers Mark D MD Gavrilin Mikhail A MA Ross Patrick P Abbas Abbas A Eng Charis C

American journal of respiratory and critical care medicine 20090212 10

<h4>Rationale</h4>Little is known about the genetic regulation of granulomatous inflammation in sarcoidosis.<h4>Objectives</h4>To determine if tissue gene array analysis would identify novel genes engaged in inflammation and lung remodeling in patients with sarcoidosis.<h4>Methods</h4>Gene expression analysis was performed on tissues obtained from patients with sarcoidosis at the time of diagnosis (untreated) (n = 6) compared with normal lung tissue (n = 6). Expression of select genes was furthe ...[more]

PMID: 19218196

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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.

Dataset Information

Genome-wide gene expression profile analysis in pulmonary sarcoidosis

Publications

Gene expression profiling identifies MMP-12 and ADAMDEC1 as potential pathogenic mediators of pulmonary sarcoidosis.

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