Microarray for Genes Associated with Signal Transduction in Diabetic OLETF Keratocytes
Korean Journal of Ophthalmology
;
: 111-119, 2007.
Artigo
em Inglês
| WPRIM
| ID: wpr-115058
ABSTRACT
PURPOSE:
The purpose of this study was to identify differences in signal transduction gene expression between normal and diabetic keratocytes stimulated with interleukin-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha).METHODS:
Normal and diabetic keratocytes were primarily cultured and treated with 20 ng/ml IL-1alpha and TNF-alpha for 6 h. cDNA was hybridized to an oligonucleotide microarray. Genes identified by the microarray were further evaluated by real-time PCR.RESULTS:
Diabetic keratocytes over-expressed components of the MAPK and Notch pathways, and under-expressed components of the insulin, calcium, and TGF-beta pathways. Cytokine treated diabetic keratocytes differentially expressed components of the TGF-beta and MAPK pathways. After IL-1alpha and TNF-alpha treatment, nine genes were under-expressed, falling in the insulin, TGF-beta, and Toll-like receptor pathways. Real-time PCR showed a significant decrease in the IL-6 and TGF-beta2 genes and a significant increase in the Ppm1a gene.CONCLUSIONS:
There were some differences in gene expression between normal and diabetic keratocytes related to signal transduction pathways, such as the insulin, MAPK, calcium, and TGF-beta pathways. In addition, IL-1alpha and TNF-alpha stimulating the insulin, TGF-beta, and Toll-like receptor signaling pathways may have different effects in diabetic keratocytes.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Prolactina
/
DNA
/
Proteínas Nucleares
/
Transdução de Sinais
/
Células Cultivadas
/
Reação em Cadeia da Polimerase
/
Fator de Crescimento Transformador beta
/
Fator de Necrose Tumoral alfa
/
Apoptose
/
Monoéster Fosfórico Hidrolases
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Inglês
Revista:
Korean Journal of Ophthalmology
Ano de publicação:
2007
Tipo de documento:
Artigo
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