Characterization of Differentially Expressed Genes upon Chronic Fluoxetine Treatment in Rat C6 Glioma Cells.
- Author:
Mi Ran CHOI
1
;
Seung Youn BAIK
;
Kyoung Hwa JUNG
;
Young Gyu CHAI
;
Seok Hyeon KIM
;
Sungwon ROH
;
Jun Seok LEE
;
Dong Yul OH
;
Ihn Geun CHOI
;
Byung Hwan YANG
Author Information
1. Department of Biochemistry and Molecular Biology, Hanyang University, Ansan, Korea.
- Publication Type:Original Article
- Keywords:
Fluoxetine;
Gs;
Gi2;
NCAM140
- MeSH:
Animals;
Atrophy;
DNA, Complementary;
Fluoxetine*;
Glioma*;
Neurites;
Oligonucleotide Array Sequence Analysis;
Plastics;
Rats*;
RNA;
Signal Transduction
- From:Korean Journal of Psychopharmacology
2004;15(4):457-467
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: The aim of this study was to identify diffrentially regulated genes after the treatment of fluoxetine in rat C6 glioma cells using cDNA microarray chip techniques and real-time RT-PCR. METHODS: Cells were incubated for 24 hours, and for 72 hours with or without 10 uM fluoxetine. Total RNAs extracted from cells were reversely transcribed to cDNA. These cDNA were used to carry out cDNA microarray chip. A part of the up-/down-regulated genes in cDNA microarray result were confirmed by real-time RT-PCR. RESULTS: 1) Genes in fluoxetinetreated cells for 72 hours (chronic treatment) were more regulated than that in fluoxetine-treated cells for 24 hours (acute treatment). 2) The expression level of Gs gene in fluoxetine-treated cells for 24 hours hardly altered, but that of Gs in fluoxetine-treated cells for 72 hours significantly increased. The expression of Gi2 also decreased in 72 hours in relation to 24 hours after the administration of fluoxetine. 3) The expression level of NCAM140 gene in fluoxetine-treated cells was higher than that in control cells. CONCLUSION: We identified genes (Gs, Gi2 and NCAM140) related to neural plasticity and intracellular signal transduction cascade from our result. This implies that fluoxetine may inhibit atrophy or death of impaired neural cells by promoting neurite outgrowth.
