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Transcriptome analysis and gene expression profiles of early apoptosis‐related genes in Streptococcus pyogenes ‐infected epithelial cells
Author(s) -
Nakagawa Ichiro,
Nakata Masanobu,
Kawabata Shigetada,
Hamada Shigeyuki
Publication year - 2004
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2004.00412.x
Subject(s) - biology , apoptosis , gene , downregulation and upregulation , streptococcus pyogenes , microbiology and biotechnology , gene expression , transcriptome , programmed cell death , regulation of gene expression , serial analysis of gene expression , genetics , bacteria , staphylococcus aureus
Summary 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‐1β, 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.

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