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Sang June Hahn  (Hahn SJ) 2 Articles
The Role of cAMP/PKA Activation on Exendin-4-Induced Cyclin D1 Expression in INS-1 Cell.
Gyeong Ryul Ryu, Jung Hoon Kang, Hwa In Jang, Seung Hyun Ko, In Kyung Jeong, Duck Joo Rhie, Shin Hee Yoon, Sang June Hahn, Yang Hyeok Jo, Myung Suk Kim, Myung Jun Kim
Korean Diabetes J. 2005;29(4):295-303.   Published online July 1, 2005
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BACKGROUND
Glucagon-like peptide-1(GLP-1) and exendin-4(EX-4) have been known to induce pancreatic islet proliferation and increases in the betacell mass. Cyclin D1 is a key protein responsible for the entry of the G into the S phase, thereby contributing to cell proliferation. Therefore, the effect of EX-4 on the expression of cyclin D1 in INS-1 cells, a rat pancreatic betacell line, was investigated. The involvement of either mitogen-activated protein kinases(MAPKs) or cyclic adenosine 5'-monophosphate/protein kinase A(cAMP/ PKA) in the EX-4-induced cyclin D1 expression was also examined. METHODS: INS-1 cells were treated with EX-4 (10 nM), and the cyclin D1 protein levels then determined by Western blot. To investigate the involvement of MAPKs in the EX-4- induced cyclin D1 expression, either a combined treatment of MAPKs inhibitors or transient transfection of extracellular signal-regulated kinase-1 (ERK1) was performed. The effect of cAMP on the EX-4-induced cyclin D1 expression was also examined by treatments with forskolin, an adenylyl cyclase activator, and H-89, a PKA inhibitor. RESULTS: EX-4 increased the expression of cyclin D1 protein in a dose-dependent manner. Although EX-4 induced phosphorylation of ERK1/2, the treatment with PD 98059 or the overexpression of ERK1 had no effect on the EX-4-induced cyclin D1 expression. However, forskolin significantly induced the expression of cyclin D1, whereas the pretreatment of H-89 inhibited the EX-4-induced cyclin D1 expression. CONCLUSION: These results suggest that EX-4 induce cyclin D1 expression in INS-1 cells via cAMP/PKA pathway, but this is not due to ERK activation.
The Inhibitory Effect of Epicatechin on IL-1beta -induced iNOS Expression and NO Production in RINm5F Cell.
Gyeong Ryul Ryu, Do Sik Min, Duck Joo Rhie, Shin Hee Yoon, Sang June Hahn, Myung Suk Kim, Yang Hyeok Jo, Myung Jun Kim
Korean Diabetes J. 2003;27(6):456-466.   Published online December 1, 2003
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AbstractAbstract PDF
BACKGROUND
Interleukin-1beta (IL-1beta ) stimulates the expression of inducible nitric oxide synthase (iNOS) and the production of nitric oxide (NO), lead to NO-mediated insulin, which produces cell damage. Within these signal pathways, nuclear factor-kappaB (NF-kappaB) activation is crucial, with many IL-1beta -sensitive genes containing NF-kappaB binding sites in their promoter regions. The inhibitory effect of (-)epicatechin (EC), an antioxidant agent, on IL-1beta -induced NF-kappaB activation, and the subsequent iNOS expression in RINm5F cells, were examined. METHODS: RINm5F cells were pretreated with EC (0.8 mM), and then cultured with IL-1beta (10U/mL), and the iNOS mRNA and protein levels then determined by Northern and Western blots, respectively. The production of NO was measured as nitrite in the culture supernatant. The protein levels of the inhibitor of nuclear factor kappaB (IkappaB) and NF-kappaB DNA binding activity were determined by Western blot and electrophoretic mobility shift assay, respectively. Also, the promoter activity following transient transfection of the iNOS promoter-luciferase reporter genes into the cells were tested. RESULTS: EC was found to significantly reduce the IL-1beta -induced NO production, and iNOS protein and mRNA levels, and also blocked the IL-1beta -induced IkappaB protein degradation, NF-kappaB activation and iNOS promoter activity. CONCLUSION: These results suggest that EC inhibits the IL-1beta -induced iNOS expression in RINm5F cells, by interfering with the binding of the NF-kappaB to the iNOS promoter, thereby inhibiting the induction of iNOS transcription.

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