Gene expression profiles in adenosine-treated human mast cells

Abstract

The role of mast cells in allergic diseases and innate immunity has been widely researched and much is known about the expression profiles of immune-related genes in mast cells after bacterial challenges. However, little is known about the gene expression profiles of mast cells in response to adenosine. Herein, we profiled the transcriptome changes of human mast cells treated with adenosine. To perform comparative transcriptome analysis between adenosine-untreated control mast cells (MN) and adenosine-treated mast cells (MT), two independent cDNA libraries were constructed using the 5'-oligocapping method. Analysis of the 3,968 (MN, 1,994; MT, 1,974) expression sequence tags (ESTs) generated from these libraries identified 369 contigs (MN, 189; MT, 180) and 2,655 singletons (MN, 1,289; MT, 1,366) with average lengths of 668 and 655 bp, respectively. Furthermore, comparison of our EST sequences against the eukaryotic orthologous group (KOG) database showed that 2,134 (52.92%) out of 4,032 sequences could be grouped into three major functional categories. As a result of analysis at the individual level of the genes, we found that the expression of genes encoding Pdia (protein disulfide isomerase-associated), adaptor-related protein complex, ATP-dependent DNA helicase II, cyclin M4, reticulon 3 isoform, CD37 antigen isoform A, glutamine synthetase, WD repeat domain, programmed cell death and proliferating cell nuclear antigen increased by 4-fold. In contrast, the expression of genes encoding thymosin beta 4, ring finger protein, high-mobility group, calmodulin 2, RAN binding protein, solute carrier family 25, tubulin alpha and peroxiredoxin decreased by 4-fold. Information obtained from our study will enhance the understanding of defense mechanisms associated with innate immune responses by human mast cells, for which identification of immune regulators of those genes is required.

Key words: Mast cells, adenosine, expression sequence tags (EST).