Involvement of Intracellular Ca(2+)-and PI3K-Dependent ERK Activation in TCDD-Induced Inhibition of Cell Proliferation in SK-N-SH Human Neuronal Cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yang, Seun-Ah | - |
dc.contributor.author | Lee, Yong-Soo | - |
dc.contributor.author | Jin, Da-Qing | - |
dc.contributor.author | Jung, Jae-Wook | - |
dc.contributor.author | Park, Byung-Chul | - |
dc.contributor.author | Lee, Yoon-Seok | - |
dc.contributor.author | Paek, Seung-Hwan | - |
dc.contributor.author | Jeong, Tae-Cheon | - |
dc.contributor.author | Choi, Han-Gon | - |
dc.contributor.author | Yong, Chul-Soon | - |
dc.contributor.author | Yoo, Bong-Kyu | - |
dc.contributor.author | Kim, Jung-Ae | - |
dc.date.accessioned | 2021-06-23T23:39:15Z | - |
dc.date.available | 2021-06-23T23:39:15Z | - |
dc.date.created | 2021-02-18 | - |
dc.date.issued | 2005-04 | - |
dc.identifier.issn | 1976-9148 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/46027 | - |
dc.description.abstract | 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has previously shown to induce neurotoxicity through intracellular Ca2+ increase in rat neurons. In this study we investigated the role and signaling pathway of intracellular Ca2+ in TCDD-induced inhibition of neuronal cell proliferation in SK-N-SH human neuronal cells. We found that TCDD (10 nM) rapidly increased the level of intracellular Ca2+, which was completely blocked by the extracellular Ca2+ chelation with EGTA (1 mM) or by pretreatment of the cells with the non-selective cation channel blocker, flufenamic acid (200 M). However, pretreatment of the cells with dantrolene (25 M) and TMB-8 (10 M), intracellular Ca2+-release blockers, or a voltage-sensitive Ca2+ channel blocker, verapamil (100 M), failed to block the TCDD-induced Ca2+ increase in the cells. In addition, TCDD induced a rapid and transient activation of phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase1/2 (ERK1/2), which was significantly blocked by the pretreatment with BAPTA, an intracellular Ca2+ chelator, and LY294002, a PI3K inhibitor. Furthermore, inhibitors of PI3K, ERK, or an intracellular Ca2+ chelator further potentiated the anti-proliferative effect of TCDD in the cells. Collectively, the results suggest that intracellular Ca2+ and PI3K-dependent activation of ERK1/2 may be involved in the TCDD-induced inhibition of cell proliferation in SK-N-SH human neuronal cells | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | 한국응용약물학회 | - |
dc.title | Involvement of Intracellular Ca(2+)-and PI3K-Dependent ERK Activation in TCDD-Induced Inhibition of Cell Proliferation in SK-N-SH Human Neuronal Cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Choi, Han-Gon | - |
dc.identifier.bibliographicCitation | 응용약물학회지(Biomolecules & Therapeutics), v.13, no.2, pp.78 - 83 | - |
dc.relation.isPartOf | 응용약물학회지(Biomolecules & Therapeutics) | - |
dc.citation.title | 응용약물학회지(Biomolecules & Therapeutics) | - |
dc.citation.volume | 13 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 78 | - |
dc.citation.endPage | 83 | - |
dc.type.rims | ART | - |
dc.identifier.kciid | ART001114546 | - |
dc.description.journalClass | 2 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | kci | - |
dc.subject.keywordAuthor | TCDD | - |
dc.subject.keywordAuthor | neurotoxicity | - |
dc.subject.keywordAuthor | intracellular Ca(2+) | - |
dc.subject.keywordAuthor | ERK | - |
dc.subject.keywordAuthor | PI3K | - |
dc.subject.keywordAuthor | proliferation | - |
dc.subject.keywordAuthor | SK-N-SH human neuronal cells | - |
dc.identifier.url | https://www.koreascience.or.kr/article/JAKO200508824144933.page | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
55 Hanyangdeahak-ro, Sangnok-gu, Ansan, Gyeonggi-do, 15588, Korea+82-31-400-4269 sweetbrain@hanyang.ac.kr
COPYRIGHT © 2021 HANYANG UNIVERSITY. ALL RIGHTS RESERVED.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.