Cited 12 times in
Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS
DC Field | Value | Language |
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dc.contributor.author | 민아림 | - |
dc.contributor.author | 신명헌 | - |
dc.contributor.author | 이영아 | - |
dc.date.accessioned | 2014-12-18T08:28:59Z | - |
dc.date.available | 2014-12-18T08:28:59Z | - |
dc.date.issued | 2013 | - |
dc.identifier.issn | 0023-4001 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/86391 | - |
dc.description.abstract | Entamoeba histolytica, which causes amoebic colitis and occasionally liver abscess in humans, is able to induce host cell death. However, signaling mechanisms of colon cell death induced by E. histolytica are not fully elucidated. In this study, we investigated the signaling role of NOX in cell death of HT29 colonic epithelial cells induced by E. histolytica. Incubation of HT29 cells with amoebic trophozoites resulted in DNA fragmentation that is a hallmark of apoptotic cell death. In addition, E. histolytica generate intracellular reactive oxygen species (ROS) in a contact-dependent manner. Inhibition of intracellular ROS level with treatment with DPI, an inhibitor of NADPH oxidases (NOXs), decreased Entamoeba-induced ROS generation and cell death in HT29 cells. However, pan-caspase inhibitor did not affect E. histolytica-induced HT29 cell death. In HT29 cells, catalytic subunit NOX1 and regulatory subunit Rac1 for NOX1 activation were highly expressed. We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Suppression of Rac1 by siRNA significantly inhibited Entamoeba-induced cell death. Moreover, knockdown of NOX1 by siRNA, effectively inhibited E. histolytica-triggered DNA fragmentation in HT29 cells. These results suggest that NOX1-derived ROS is required for apoptotic cell death in HT29 colon epithelial cells induced by E. histolytica. | - |
dc.description.statementOfResponsibility | open | - |
dc.relation.isPartOf | KOREAN JOURNAL OF PARASITOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Environmental Medical Biology (환경의생물학) | - |
dc.contributor.googleauthor | Kyeong Ah Kim | - |
dc.contributor.googleauthor | Ju Young Kim | - |
dc.contributor.googleauthor | Young Ah Lee | - |
dc.contributor.googleauthor | Arim Min | - |
dc.contributor.googleauthor | Young Yil Bahk | - |
dc.contributor.googleauthor | Myeong Heon Shin | - |
dc.identifier.doi | 10.3347/kjp.2013.51.1.61 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01405 | - |
dc.contributor.localId | A02099 | - |
dc.contributor.localId | A02959 | - |
dc.relation.journalcode | J01957 | - |
dc.identifier.eissn | 1738-0006 | - |
dc.identifier.pmid | Entamoeba histolytica ; host cell death ; HT29 colon epithelial cell ; reactive oxygen species (ROS) ; NADPH oxidase 1 (NOX1) | - |
dc.subject.keyword | Entamoeba histolytica | - |
dc.subject.keyword | host cell death | - |
dc.subject.keyword | HT29 colon epithelial cell | - |
dc.subject.keyword | reactive oxygen species (ROS) | - |
dc.subject.keyword | NADPH oxidase 1 (NOX1) | - |
dc.contributor.alternativeName | Min, A Rim | - |
dc.contributor.alternativeName | Shin, Myeong Heon | - |
dc.contributor.alternativeName | Lee, Young Ah | - |
dc.contributor.affiliatedAuthor | Min, A Rim | - |
dc.contributor.affiliatedAuthor | Shin, Myeong Heon | - |
dc.contributor.affiliatedAuthor | Lee, Young Ah | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 51 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 61 | - |
dc.citation.endPage | 68 | - |
dc.identifier.bibliographicCitation | KOREAN JOURNAL OF PARASITOLOGY, Vol.51(1) : 61-68, 2013 | - |
dc.identifier.rimsid | 28953 | - |
dc.type.rims | ART | - |
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