Microarray analysis of eosinophils reveals a number of candidate survival and apoptosis genes

Temple, R., Allen, E., Fordham, J., Phipps, S., Schneider, H. C., Lindauer, K., Hayes, I., Lockey, J., Pollock, K. and Jupp, R. (2001) Microarray analysis of eosinophils reveals a number of candidate survival and apoptosis genes. American Journal of Respiratory Cell and Molecular Biology, 25 4: 425-433. doi:10.1165/ajrcmb.25.4.4456


Author Temple, R.
Allen, E.
Fordham, J.
Phipps, S.
Schneider, H. C.
Lindauer, K.
Hayes, I.
Lockey, J.
Pollock, K.
Jupp, R.
Title Microarray analysis of eosinophils reveals a number of candidate survival and apoptosis genes
Journal name American Journal of Respiratory Cell and Molecular Biology   Check publisher's open access policy
ISSN 1044-1549
1535-4989
Publication date 2001-10-01
Year available 2001
Sub-type Article (original research)
DOI 10.1165/ajrcmb.25.4.4456
Open Access Status Not yet assessed
Volume 25
Issue 4
Start page 425
End page 433
Total pages 9
Place of publication New York, NY, United States
Publisher American Thoracic Society
Language eng
Abstract The increase in eosinophils at the site of antigen challenge has been used as evidence to suggest that this cell type plays a role in the pathophysiology of asthma. Aberrant production of several different cytokines, particularly interleukin (IL)-5, has been shown to result in eosinophilia. IL-5 influences the development and maturation of eosinophils in a number of different ways. Of note is the ability of IL-5 to act as a survival factor for eosinophils specifically inhibiting apoptosis. The precise mechanism by which IL-5 exerts its effect remains obscure. We used microarray technologies to investigate the changes in the messenger RNA expression profile of eosinophils after treatment with IL-5. Using the Affymetrix Hu6800 chip, a total of 80 genes were observed to be regulated by 2-fold or greater. Many of the genes previously identified as regulated by IL-5 were regulated in our microarray experiments. Of the 73 genes found to be upregulated, many were shown to play a role in adhesion, migration, activation, or survival of eosinophils or hematopoietic cells, whereas the function of others was unknown. To facilitate the identification of genes that govern the apoptosis and survivability of eosinophils, we used an alternative cellular model, TF1.8 cells, whose survival was also dependent on IL-5. Comparison of these models identified four genes, Pim-1, DSP-5 (hVH3, B23), CD24, and SLP-76, whose regulation was similarly coordinated in both systems. identification of Pim-1 and SLP-76 as regulated by IL-5 led us to suggest a direct role for these proteins in the IL-5 signaling pathway in eosinophils. The tissue distribution of these genes demonstrated that Pim-1 and SLP-76 were relatively restricted to the eosinophil compared with their expression in rain bone marrow, kidney, liver, and lung. By contrast, DSP-5 and CD24 were confirmed as ubiquitous in their expression by microarray.
Formatted abstract
The increase in eosinophils at the site of antigen challenge has been used as evidence to suggest that this cell type plays a role in the pathophysiology of asthma. Aberrant production of several different cytokines, particularly interleukin (IL)-5, has been shown to result in eosinophilia. IL-5 influences the development and maturation of eosinophils in a number of different ways. Of note is the ability of IL-5 to act as a survival factor for eosinophils specifically inhibiting apoptosis. The precise mechanism by which IL-5 exerts its effect remains obscure. We used microarray technologies to investigate the changes in the messenger RNA expression profile of eosinophils after treatment with IL-5. Using the Affymetrix Hu6800 chip, a total of 80 genes were observed to be regulated by 2-fold or greater. Many of the genes previously identified as regulated by IL-5 were regulated in our microarray experiments. Of the 73 genes found to be upregulated, many were shown to play a role in adhesion, migration, activation, or survival of eosinophils or hematopoietic cells, whereas the function of others was unknown. To facilitate the identification of genes that govern the apoptosis and survivability of eosinophils, we used an alternative cellular model, TF1.8 cells, whose survival was also dependent on IL-5. Comparison of these models identified four genes, Pim-1, DSP-5 (hVH3, B23), CD24, and SLP-76, whose regulation was similarly coordinated in both systems. Identification of Pim-1 and SLP-76 as regulated by IL-5 led us to suggest a direct role for these proteins in the IL-5 signaling pathway in eosinophils. The tissue distribution of these genes demonstrated that Pim-1 and SLP-76 were relatively restricted to the eosinophil compared with their expression in brain, bone marrow, kidney, liver, and lung. By contrast, DSP-5 and CD24 were confirmed as ubiquitous in their expression by microarray.
Keyword Biochemistry & Molecular Biology
Cell Biology
Respiratory System
Biochemistry & Molecular Biology
Cell Biology
Respiratory System
BIOCHEMISTRY & MOLECULAR BIOLOGY
CELL BIOLOGY
RESPIRATORY SYSTEM
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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Created: Thu, 10 Mar 2011, 00:32:14 EST