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Gene expression profiling of human calcific aortic valve disease.

ABSTRACT: Calcific aortic valve disease is a slowly progressive disorder that ranges from mild valve thickening (i.e. aortic sclerosis) to severe calcification of valves (i.e. aortic stenosis). Gene expression profiling analysis of non-calcified controls, sclerotic, and calcified aortic valves was performed to better understand the progression of calcific aortic valve disease. The complementary information related to processing and statistical analysis of the DNA microarray data is provided in this article. Interpretation of this data can be found in a research article entitled "MicroRNA-125b and chemokine CCL4 expression are associated with calcific aortic valve disease" [1]. The microarray data complies with MIAME guidelines and is deposited in the Gene Expression Omnibus (GEO) database under accession number GSE51472.

SUBMITTER: Rysa J

PROVIDER: S-EPMC4778651 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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Gene expression profiling of human calcific aortic valve disease.

Rysä Jaana J

Genomics data 20151219

Calcific aortic valve disease is a slowly progressive disorder that ranges from mild valve thickening (i.e. aortic sclerosis) to severe calcification of valves (i.e. aortic stenosis). Gene expression profiling analysis of non-calcified controls, sclerotic, and calcified aortic valves was performed to better understand the progression of calcific aortic valve disease. The complementary information related to processing and statistical analysis of the DNA microarray data is provided in this articl ...[more]

PMID: 26981379

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The alterations of gene expression in aortic valve from calcific aortic valve disease patients

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Transcriptional Profiles of Aortic Valve from Calcific Aortic Valve Disease and Normal Control.

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Inhibitory Role of Notch1 in Calcific Aortic Valve Disease

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Adaptive immune cells in calcific aortic valve disease.

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Identification of key genes in calcific aortic valve disease via weighted gene co-expression network analysis.

Project description:BackgroundCalcific aortic valve disease (CAVD) is the most common subclass of valve heart disease in the elderly population and a primary cause of aortic valve stenosis. However, the underlying mechanisms remain unclear.MethodsThe gene expression profiles of GSE83453, GSE51472, and GSE12644 were analyzed by 'limma' and 'weighted gene co-expression network analysis (WGCNA)' package in R to identify differentially expressed genes (DEGs) and key modules associated with CAVD, respectively. Then, enrichment analysis was performed based on Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, DisGeNET, and TRRUST database. Protein-protein interaction network was constructed using the overlapped genes of DEGs and key modules, and we identified the top 5 hub genes by mixed character calculation.ResultsWe identified the blue and yellow modules as the key modules. Enrichment analysis showed that leukocyte migration, extracellular matrix, and extracellular matrix structural constituent were significantly enriched. SPP1, TNC, SCG2, FAM20A, and CD52 were identified as hub genes, and their expression levels in calcified or normal aortic valve samples were illustrated, respectively.ConclusionsThis study suggested that SPP1, TNC, SCG2, FAM20A, and CD52 might be hub genes associated with CAVD. Further studies are required to elucidate the underlying mechanisms and provide potential therapeutic targets.

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Inhibitory role of Notch1 in calcific aortic valve disease.

Project description:Aortic valve calcification is the most common form of valvular heart disease, but the mechanisms of calcific aortic valve disease (CAVD) are unknown. NOTCH1 mutations are associated with aortic valve malformations and adult-onset calcification in families with inherited disease. The Notch signaling pathway is critical for multiple cell differentiation processes, but its role in the development of CAVD is not well understood. The aim of this study was to investigate the molecular changes that occur with inhibition of Notch signaling in the aortic valve. Notch signaling pathway members are expressed in adult aortic valve cusps, and examination of diseased human aortic valves revealed decreased expression of NOTCH1 in areas of calcium deposition. To identify downstream mediators of Notch1, we examined gene expression changes that occur with chemical inhibition of Notch signaling in rat aortic valve interstitial cells (AVICs). We found significant downregulation of Sox9 along with several cartilage-specific genes that were direct targets of the transcription factor, Sox9. Loss of Sox9 expression has been published to be associated with aortic valve calcification. Utilizing an in vitro porcine aortic valve calcification model system, inhibition of Notch activity resulted in accelerated calcification while stimulation of Notch signaling attenuated the calcific process. Finally, the addition of Sox9 was able to prevent the calcification of porcine AVICs that occurs with Notch inhibition. In conclusion, loss of Notch signaling contributes to aortic valve calcification via a Sox9-dependent mechanism.

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