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여말희 ( Marie Yeo ),조성원 ( Sung Won Cho ),함기백 ( Ki Baik Hahm ) 대한소화기학회 2004 대한소화기학회지 Vol.44 No.5
In the post-genomic era, the focus of research is now moving to functional genomics employing the information on predicted gene products provided by genome sequencing. Proteomics, the global analysis of structures, functions, and interactions of whole cel
에 의한 위암세포주 사멸에서 Caspase - 3 와 Mitogen - activated Protein Kinase 활성화의 역할
김원호(Won Ho Kim),진수현(Soo Hyun Jin),김태일(Tae Il Kim),여말희(Marie Yeo),최종원(Jong Won choi),김 철(Chui Kim) 대한소화기학회 2001 대한소화기학회지 Vol.37 No.6
Background/Aims: Apoptosis is one of the important mechanisms of Helicobacter pylori (H. pylori)-induced epithelial cell damage. We have attempted to demonstrate the role of mitogen-activated protein (MAP) kinases in H. pylori-induced apoptosis in gastric cancer cell. Methods: H. pylori (ATCC 43504) and AGS cell line were used. Cell survival and death were assessed by MTT assay and trypan blue dye exclusion method. Apoptosis was detected by demonstration of DNA fragmentation in agarose gel electrophoresis. Caspase-3 activity was measured by a cleavage of fluorogenic substrate, Ac-DEVD-AMC. The activation of MAP kinase was assessed by Western blot. SB203580, PD98059 and Ac-DEVD-CHO were used for the inhibition of p38 kinase, ERK and caspase-3, respectively. Results: H. pylori-induced significant cell death, the caspase-3 activation, and DNA fragmentation in AGS cells, were accompanied by the activation of all three MAP kinase subfamilies. DNA fragmentation was attenuated by Ac-DEVD-CHO, an inhibitor of caspase-3. SB203580 reduced H. pylori-induced cell death by 42.6 while PD098059 did not affect cell death. However, caspase-3 and p38 kinase were not significantly inter-linked in H. pylori-induced apoptosis. Conclusions: These results suggest that H. pylori induce the activation of MAP kinases in AGS cells and especially, the activation of p38 kinase may play a partial but significant role in H. pylori-induced apoptosis. (Korean J Gastroenterol 2001;37:418-427)
Helicobater pylori에 의한 위암세포주 사멸
김원호,이경원,박인서,이용찬,여말희,이꽃실 대한소화기학회 1999 대한소화기학회지 Vol.34 No.1
Background/Aims: Helicobacter pylori (H. pylori) is associated with active gastritis and peptic ulcer disease. Mechanism for H. pylori-induced gastric epithelial damage is still incompletely understood. However, the increase of apoptotic cells in H. pylori-infected mucosa suggested that apoptosis could be a major mechanism for cellular damage. As an effort to clarify the mechanism, we investigated whether H. pylori directly induce apoptosis in gastric cancer cells in vitro. Methods: Cultured H. pylori (ATCC 43504) were suspended as 109/mL. IL (interleukin)-8 was measured by enzyme linked immunosorbent assay. Cell survival was assessed by MTT [3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Apoptosis was detected and confirmed by demonstration of DNA fragmentation and morphologic changes. Results: H. pylori induced IL-8 production as well as decrease of cell survival in gastric cancer cell lines in a time- and concentration-dependen way. Addition of H. pylori to gastric cancer cells induced apoptosis. Such induction was not organ specific. Heat or formalin treatment of H. pylori almost completely inhibited IL-8 production but only partially blocked apoptosis. H. pylori- induced apoptosis was potentiated by interferon-γ pretreatment in HT-29 but not in AGS and KATO III. Conclusions: These results suggest that H. pylori affects on gastric epithelial cell growth by direct induction of apoptosis.