연구성과물 검색 타이틀 이미지

HOME ICON HOME > Search by Achievements Type > Reports View

Reports Detailed Information
Apoptosis of Gastric Epithelial Cell by Helicobacter pylori γ-glutamyltranspeptidase (GGT)
Reports NRF is supported by Research Projects( Apoptosis of Gastric Epithelial Cell by Helicobacter pylori γ-glutamyltranspeptidase (GGT) | 2005 Year 신청요강 다운로드 PDF다운로드 | 김경미(경상대학교(칠암)) ) data is submitted to the NRF Project Results
Researcher who has been awarded a research grant by Humanities and Social Studies Support Program of NRF has to submit an end product within 6 months(* depend on the form of business)
사업별 신청요강보기
  • Researchers have entered the information directly to the NRF of Korea research support system
Project Number C00030
Year(selected) 2005 Year
the present condition of Project 종료
State of proposition 재단승인
Completion Date 2008년 10월 31일
Year type 결과보고
Year(final report) 2008년
Research result report
  • Abstract
  • ??-Glutamyltranspeptidase (GGT) is a novel protein in the induction of H. pylori-mediated apoptosis; however, the signal pathway involved in GGT-induced apoptosis remains unclear. Using DNA recombination techniques, ggt was cloned into pET117b and transformed into E. coli. rGGT was purified using nickel-affinity resin. rGGT induced apoptosis in AGS cells in a time-dependent manner, which was confirmed by TUNEL staining, the MTT assay and immunoblot analysis for caspases-9, -3, Bax, Bcl-2, Bcl-xL and cytochrome c release. Activation of caspase-3, and -9 following exposure to GGT increased in a time-dependent manner. In addition, upregulation of proapoptotic Bax and a downregulation of antiapoptotic Bcl-2 and Bcl-xL were detected.
    Apoptotic signals also trigger changes in mitochondria, which lead to a release of cytochrome c into the cytosolic space. The ggt-deficient mutant was not as able to induce apoptosis as the wild-type strain. These results indicated that GGT of H. pylori induces apoptosis via a mitochondria-mediated pathway.
    Fallowing study was carried out to demonstrate the role of mitogen-activated protein (MAP) kinase in H. pylori GGT-induced apoptosis in AGS cells. The activation of MAP kinase was confirmed by western blot. In an attempt to elucidate the pathway, the cells were treated with PD98059, SB203580 and SP600125 for the inhibition of ERK, p38 kinase and JNK, respectively, prior to exposure to the rGGT protein. Data showed that ERK was phosphorylated and GGT-induced apoptosis was inhibited by PD98059.
    To better understand the mechanism of apoptosis by H. pylori GGT, cell cycle-related events were examined following exposure to the rGGT protein. During co-culture, H. pylori rGGT inhibited cell cycle progression at G1-S in AGS cells which were confirmed by immunoblotting analysis for CDK4, CDK6, cyclin A, cyclin E, p21, and p27. p21and p27 were up-regulated and CDK4, CDK6, cyclin A and cyclin E were down-regulated. These results indicated that rGGT inhibits cell cycle progression at G1-S for apoptosis.
    In conclusion, H. pylori rGGT induces apoptosis and inhibits cell cycle progression at G1-S, in association with ERK phosphorylation, caspase-3 activation, cytochrome c release in AGS cells.
  • Research result and Utilization method
  • H. pylori GGT가 세포자멸사를 유도한다는 최근의 보고가 있지만 그 기전에 대해서는 아직 알려진 바가 없다. H. pylori의 발병결정인자로 잘 알려진 GGT가 유도하는 세포자멸사 기전에 대한 연구가 필요하다고 판단되어 위상피세포에 H. pylori GGT 재조합단백질을 처리하였을 때 재조합 GGT 단백질이 세포자멸사를 유도하는 신호전달 과정 중에 AGS 세포는 GGT에 의하여 세포주기를 조절하는 단백질인 p21의 발현이 증가하였으며 미토콘드리아를 경유하여 세포질 내로의 시토크롬 c의 방출이 시간의존적으로 증가하고, caspase-3, 9의 활성을 통해 세포자멸사에 이르는 현상을 관찰할 수 있었으며 ERK 1/2의 활성화가 매개체로 작용할 것이라는 결론을 얻었다.
  • Index terms
  • H. pylori, GGT, apoptosis
  • List of digital content of this reports
데이터를 로딩중 입니다.
  • This document, it is necessary to display the original author and you do not have permission
    to use copyrighted material for-profit
  • In addition , it does not allow the change or secondary writings of work
데이터 이용 만족도
자료이용후 의견
트위터 페이스북
NRF Daejeon
(34113) 201, Gajeong-ro, Yuseong-gu, Daejeon, Korea
Tel: 82-42-869-6114 / Fax: 82-42-869-6777
NRF Seoul
(06792) 25, Heonreung-ro, Seocho-gu, Seoul, Korea
Tel: 82-2-3460-5500 / Fax: 82-2-3460-5759
KRM Help Center
Tel : 042-710-4360
E-mail : / Fax : 042-861-4380