Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김정목 | - |
dc.date.accessioned | 2022-03-18T02:17:44Z | - |
dc.date.available | 2022-03-18T02:17:44Z | - |
dc.date.issued | 2020-07 | - |
dc.identifier.citation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v. 21, no. 15, article no. 5383 | en_US |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.issn | 1422-0067 | - |
dc.identifier.uri | https://www.mdpi.com/1422-0067/21/15/5383 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/169201 | - |
dc.description.abstract | EnterotoxigenicBacteroides fragilisis a causative agent of colitis and secrets enterotoxin (BFT), leading to the disease. Sulfiredoxin (Srx)-1 serves to protect from oxidative damages. Although BFT can generate reactive oxygen species in intestinal epithelial cells (IECs), no Srx-1 expression has been reported in ETBF infection. In this study, we explored the effects of ETBF-produced BFT on Srx-1 induction in IECs. Treatment of IECs with BFT resulted in increased expression of Srx-1 in a time-dependent manner. BFT treatment also activated transcriptional signals including Nrf2, AP-1 and NF-kappa B, and the Srx-1 induction was dependent on the activation of Nrf2 signals. Nrf2 activation was assessed using immunoblot and Nrf2-DNA binding activity and the specificity was confirmed by supershift and competition assays. Suppression of NF-kappa B or AP-1 signals did not affect the upregulation of Srx-1 expression. Nrf2-dependent Srx-1 expression was associated with the activation of p38 mitogen-activated protein kinases (MAPKs) in IECs. Furthermore, suppression of Srx-1 significantly enhanced apoptosis while overexpression of Srx-1 significantly attenuated apoptosis during exposure to BFT. These results imply that a signaling cascade involving p38 and Nrf2 is essential for Srx-1 upregulation in IECs stimulated with BFT. Following this upregulation, Srx-1 may control the apoptosis in BFT-exposed IECs. | en_US |
dc.description.sponsorship | This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (MEST) (NRF-2018R1D1A1B07043350), Republic of Korea. | en_US |
dc.language.iso | en | en_US |
dc.publisher | MDPI | en_US |
dc.subject | Bacteroides fragilis | en_US |
dc.subject | enterotoxin | en_US |
dc.subject | intestinal epithelial cells | en_US |
dc.subject | sulfiredoxin-1 | en_US |
dc.title | Bacteroides fragilis Enterotoxin Induces Sulfiredoxin-1 Expression in Intestinal Epithelial Cell Lines Through a Mitogen-Activated Protein Kinases- and Nrf2-Dependent Pathway, Leading to the Suppression of Apoptosis | en_US |
dc.type | Article | en_US |
dc.relation.no | 15 | - |
dc.relation.volume | 21 | - |
dc.identifier.doi | 10.3390/ijms21155383 | - |
dc.relation.page | 1-16 | - |
dc.relation.journal | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.contributor.googleauthor | Jeon, Jong Ik | - |
dc.contributor.googleauthor | Choi, Jun Ho | - |
dc.contributor.googleauthor | Lee, Keun Hwa | - |
dc.contributor.googleauthor | Kim, Jung Mogg | - |
dc.relation.code | 2020050347 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jungmogg | - |
dc.identifier.orcid | https://orcid.org/0000-0002-6506-7519 | - |
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