Linked Life Data

15339269

Source:http://linkedlifedata.com/resource/pubmed/id/15339269

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2004-9-1
pubmed:abstractText
Epithelial cells are the initial sites of host invasion by group A Streptococcus pyogenes (GAS), and GAS infection of epithelial cells has been suggested to induce apoptosis. We previously reported that the induction of apoptosis is strongly associated with the protein F1-mediated invasion. We present here the gene expression profiles of the human epithelial HEp-2 cells during GAS-induced apoptosis, using serial gene analysis of expression (SAGE) analysis and macroarray analysis of apoptosis-related genes. Serial gene analysis of expression revealed the downregulation of voltage-dependent anion channels 1 and 2 genes and the upregulation of the cytochrome c oxidase and calcium binding protein genes (calpactin, calgizzarin and programmed cell death 6). Macroarray analysis and quantitative RT-PCR analysis also revealed that the genes for IL-1beta, IL-12 p35, IL12 p40, and GM-CSF are also markedly induced by GAS invasion. Furthermore, caspase-1, -9, and -14 genes are significantly upregulated during GAS invasion. These observations indicated that apoptosis associated with GAS invasion is mainly induced by mitochondrial dysfunction and calcium regulation as well as by stress, and that these transcriptional controls may regulate the cellular response to GAS invasion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1462-5814
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
939-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Transcriptome analysis and gene expression profiles of early apoptosis-related genes in Streptococcus pyogenes-infected epithelial cells.
pubmed:affiliation
Department of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita-Osaka, Japan. ichiro@dent.osaka-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't