Analysis of Microarray Experiments for Pulmonary Fibrosis

Dave, Nilesh B.; Kaminski, Naftali

doi:10.1385/1-59259-940-0:333

Cited by 15 publications

(17 citation statements)

References 9 publications

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“…nih.gov/geo) according to minimal information about microarray experiments (MIAME) guidelines. The general approach to analysis has been previously described by us (30). Correction for multiple testing was performed by calculating the false discovery rate, as previously described (30).…”

Section: Microarray Analysismentioning

confidence: 99%

“…The general approach to analysis has been previously described by us (30). Correction for multiple testing was performed by calculating the false discovery rate, as previously described (30). Genes were defined as being substantially changed if they had a threshold number of misclassifications (TNoM) score of 0 and a t test with a P value of less than 0.05, as previously described (31).…”

Section: Microarray Analysismentioning

confidence: 99%

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WNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis

Vuga¹,

Ben‐Yehudah²,

Kovkarova-Naumovski³

et al. 2009

Am J Respir Cell Mol Biol

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Usual interstitial pneumonia (UIP) is a specific histopathologic pattern of interstitial lung fibrosis that may be idiopathic or secondary to autoimmune diseases and environmental exposures. In this study, we compared gene expression patterns in primary fibroblasts isolated from lung tissues with UIP histology and fibroblasts isolated from lung tissues with normal histology using expression microarrays. We found that WNT5A was significantly increased in fibroblasts obtained from UIP lung tissues compared with normal lung fibroblasts, an observation verified by quantitative real-time RT-PCR and Western blot. Because the role of WNT5A in UIP is unknown, we treated normal lung fibroblasts or UIP lung fibroblasts with WNT5A, and found that WNT5A increased proliferation as well as relative resistance to H 2 O 2 -induced apoptosis. This effect was not mediated through the canonical WNT/b-catenin pathway, as WNT5A induced a decrease in b-catenin levels in the same cells. In addition, WNT5A induced increases in fibronectin and a 5 -integrin in normal lung fibroblasts. Collectively, our data suggest that WNT5A may play a role in fibroblast expansion and survival characteristics of idiopathic pulmonary fibrosis and other fibrotic interstitial lung diseases that exhibit UIP histological patterns.

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Section: Microarray Analysismentioning

confidence: 99%

Section: Microarray Analysismentioning

confidence: 99%

WNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis

Vuga¹,

Ben‐Yehudah²,

Kovkarova-Naumovski³

et al. 2009

Am J Respir Cell Mol Biol

Self Cite

198

179

View full text Add to dashboard Cite

show abstract

“…Encouraged by these results, and especially for this article, we reanalyzed the data using Genomica (http://genomica.weizmann.ac.il/index.html), a more advanced analysis and visualization tool, which evolved from the GeneXpress and allows integration of multiple levels of information (15,32) in analysis of high-throughput data. For each gene, we generated attribute files that included its GO annotation and its involvement in known pathways.…”

Section: Microarray Analysis Of Whole Human Ipf Lungsmentioning

confidence: 99%

“…genmapp.org/), and others, as well literature information. One of the advantages of Genomica is the simplicity by which information files can be generated (32). We then looked for enrichment of these annotations in the genes that distinguished IPF, HP, and NSIP (normal controls were not included in this analysis).…”

Section: Microarray Analysis Of Whole Human Ipf Lungsmentioning

confidence: 99%

Towards Systems Biology of Human Pulmonary Fibrosis

Studer

Kaminski²

2007

Proceedings of the American Thoracic Society

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The integrated effect of multiple pathways, molecules, genetic polymorphisms, environmental stimuli, and possible infection determines the lung phenotype in idiopathic pulmonary fibrosis (IPF), a chronic progressive and often lethal lung disease. Systems biology approaches aim to provide a systemwide view of biological process using computational tools and high-throughput technologies. Although much of the analysis of genome-level transcriptional highresolution profiles of IPF was reductionist, usually focusing on a single factor in the disease process, there are some studies that implement systems approaches. We discuss these analyses and provide examples of the global analysis of IPF, hypersensitivity pneumonitis, and nonspecific interstitial pneumonia. Detailed quantitative phenotyping and correlation with microarray results as well as highthroughput genotyping should provide us with the datasets to implement systems biology approaches in fibrosis research. Interdisciplinary teams and training of junior investigators in the vocabulary of systems biology should allow us to use these datasets integratively and generate a global model of human pulmonary fibrosis.

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“…In the systems approach, all of these types of information are downloaded and used to create gene attribute files that allow functional characterization of the biological question at hand. This approach has been reviewed previously by us (18), and the software tools for this approach have been described by us (19). What is often neglected is that experiments can also have multiple descriptors (e.g., demographics, dates of experiments, or clinical characteristics).…”

Section: A Conceptual Framework For Analysis Of Microarray Experimentsmentioning

confidence: 99%

Gene Expression Profiling as a Window into Idiopathic Pulmonary Fibrosis Pathogenesis: Can We Identify the Right Target Genes?

Kaminski¹

2006

Proceedings of the American Thoracic Society

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Expression microarrays that provide genome-level, transcriptional, high-resolution profiles have been applied successfully to multiple diseases. Although microarrays provide information regarding thousands of genes, many investigators prefer to focus on a single gene and validate its role, an approach often supported by grant and journal reviewers. Only a minority of investigators focus on global changes in gene expression. Here, we describe and contrast two general approaches to the use of microarray data: the reductionist "cherry picking" approach and the more global, quantitative "systems" approach. We describe microarray analysis experiments relevant to idiopathic pulmonary fibrosis (IPF) in the context of these two approaches. Although it seems that the cherry-picking approaches have been successful in identifying new relevant genes in IPF, we suggest that to fulfill the discovery potential of microarrays in IPF and to create a working model of IPF, unbiased integrative systems approaches are required.

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Analysis of Microarray Experiments for Pulmonary Fibrosis

Cited by 15 publications

References 9 publications

WNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis

WNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis

Towards Systems Biology of Human Pulmonary Fibrosis

Gene Expression Profiling as a Window into Idiopathic Pulmonary Fibrosis Pathogenesis: Can We Identify the Right Target Genes?

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