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Genes related with apoptosis by inflammation in diabetic keratocytes
The goal of this study was to identify the differences in apoptosis-related gene expression between normal and diabetic keratocytes stimulated with IL-1a and TNF-alpha. Primary cultured normal and diabetic keratocytes were treated with IL-1a and TNF-alpha. The cDNA from these cells was hybridized to...
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Published in: | Genes & genomics 2015, 37(7), , pp.607-614 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | The goal of this study was to identify the differences in apoptosis-related gene expression between normal and diabetic keratocytes stimulated with IL-1a and TNF-alpha. Primary cultured normal and diabetic keratocytes were treated with IL-1a and TNF-alpha. The cDNA from these cells was hybridized to an oligonucleotide microarray. Microarray analysis was used to identify differentially expressed genes, which were further evaluated by real-time polymerase chain reaction. Diabetic keratocytes overexpressed vital components of cell division, migration, and differentiation, including Ppm1a, Ncam1, and Capn9, and under-expressed components related to prevention of apoptosis, including Clu, Ptn, and Mycn. Genes commonly over-expressed in response to IL-1alpha and TNF-alpha include Siah1a, Gzmb, and Capn9. Genes underexpressed after treatment with both cytokine include Ets1, Igf1r, and Sgk. Eighteen and eight apoptosis-related genes were newly expressed after treatment with IL-1alpha and TNF-alpha, respectively. The genes commonly under-expressed after treatment with both cytokines were Bmp4 and Timp3. Real-time polymerase chain reaction showed results similar to those of the microarray analysis. IL-1alpha and TNF-alpha may modulate the expression of genes related to apoptosis in diabetic keratocytes. It may be helpful to suppress newly overexpressed genes or to enhance newly underexpressed genes by IL-1alpha or TNF-alpha for the prevention of apoptosis in keratocytes when the cornea is damaged. |
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ISSN: | 1976-9571 2092-9293 |
DOI: | 10.1007/s13258-015-0290-5 |