Linked Life Data

20114070

Source:http://linkedlifedata.com/resource/pubmed/id/20114070

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-3-15
pubmed:abstractText
Selenoprotein S (SelS), a transmembrane selenoprotein, may be related to the response of endoplasmic reticulum (ER) stress. In this report, the influence of selenite supplementation and SelS gene silence on beta-mercaptoethanol (beta-ME)-mediated ER stress and cell apoptosis in HepG2 cells were examined. The results showed that SelS protein expression was markedly increased by 10 mM beta-ME and 100 nM sodium selenite in HepG2 cells. GRP78 protein level was significantly increased after treatment with 10 mM beta-ME in HepG2 cells, which suggested that beta-ME was also an ER stress inducer. Meanwhile, beta-ME (10 mM) was found to induce cell apoptosis, which was alleviated obviously when cells were pretreated with 100 nM selenite before exposure to beta-ME. Moreover, the suppression of SelS gene by siRNA could aggravate HepG2 cell apoptosis induced by beta-ME significantly. In conclusion, these results suggested that beta-ME, also an ER stress agent, could induce cell apoptosis, and SelS may play an important role in protecting cells from apoptosis induced by ER stress in HepG2 cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-3002
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier B.V. All rights reserved.
pubmed:issnType
Print
pubmed:volume
1800
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
511-7
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Influence of SelS gene silence on beta-Mercaptoethanol-mediated endoplasmic reticulum stress and cell apoptosis in HepG2 cells.
pubmed:affiliation
Hubei Key Laboratory of Bioinorganic Chemistry & Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan 430074, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't