File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Acquired tolerance in cadmium-adapted lung epithelial cells: Roles of the c-Jun N-terminal kinase signaling pathway and basal level of metallothionein

TitleAcquired tolerance in cadmium-adapted lung epithelial cells: Roles of the c-Jun N-terminal kinase signaling pathway and basal level of metallothionein
Authors
Issue Date2006
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap
Citation
Toxicology and Applied Pharmacology, 2006, v. 215 n. 1, p. 1-8 How to Cite?
AbstractCadmium-resistant cells were developed in our laboratory with rat lung epithelial cells (LECs) by stepwise exposure of LECs to cadmium chloride from 1 microM to 20 microM after 20 passages. To investigate the Cd-resistant phenotype in a long-term perspective, cadmium-resistant cells adapted to 20 microM cadmium (Cd(R)) were then cultured in the absence of cadmium for various passages [Cd(R)(-n)]. All these adapted cells were significantly protected from cadmium toxicity as compared to parental cadmium-sensitive LECs (Cd(S)). The cadmium-resistant phenotype of adapted cells was relatively stable in the absence of cadmium for as long as 40 passages. Basal mRNA level of metallothionein-1 (MT-1) was dramatically higher in Cd(R) than in Cd(R)(-), which may account for the higher Cd-resistance of Cd(R) than Cd(R)(-). MT-1 mRNA level decreased drastically in Cd(R) after cadmium removal, suggesting that the high basal level of MT-1 in Cd(R) may be only partially responsible for cadmium-resistance. Treatment of cells with high levels of cadmium resulted in decreased phosphorylation of c-Jun N-terminal kinase (JNK1/2) in adapted cells than in sensitive cells and this cadmium-induced JNK activity was blocked by JNK inhibitor II, SP600125. Ro318220, a strong activator of JNK, reverted cadmium-sensitive phenotype in adapted cells. Taken together, our results suggest that during cadmium adaptation, cells develop tolerance to cell death, generally due to perturbation of the JNK signaling pathway and the nonresponsiveness of JNK phosphorylation is critical for the Cd-tolerance in these cells.
Persistent Identifierhttp://hdl.handle.net/10722/211386
ISSN
2015 Impact Factor: 3.847
2015 SCImago Journal Rankings: 1.593

 

DC FieldValueLanguage
dc.contributor.authorLau, TY-
dc.contributor.authorZhang, J-
dc.contributor.authorChiu, JF-
dc.date.accessioned2015-07-09T06:47:36Z-
dc.date.available2015-07-09T06:47:36Z-
dc.date.issued2006-
dc.identifier.citationToxicology and Applied Pharmacology, 2006, v. 215 n. 1, p. 1-8-
dc.identifier.issn0041-008X-
dc.identifier.urihttp://hdl.handle.net/10722/211386-
dc.description.abstractCadmium-resistant cells were developed in our laboratory with rat lung epithelial cells (LECs) by stepwise exposure of LECs to cadmium chloride from 1 microM to 20 microM after 20 passages. To investigate the Cd-resistant phenotype in a long-term perspective, cadmium-resistant cells adapted to 20 microM cadmium (Cd(R)) were then cultured in the absence of cadmium for various passages [Cd(R)(-n)]. All these adapted cells were significantly protected from cadmium toxicity as compared to parental cadmium-sensitive LECs (Cd(S)). The cadmium-resistant phenotype of adapted cells was relatively stable in the absence of cadmium for as long as 40 passages. Basal mRNA level of metallothionein-1 (MT-1) was dramatically higher in Cd(R) than in Cd(R)(-), which may account for the higher Cd-resistance of Cd(R) than Cd(R)(-). MT-1 mRNA level decreased drastically in Cd(R) after cadmium removal, suggesting that the high basal level of MT-1 in Cd(R) may be only partially responsible for cadmium-resistance. Treatment of cells with high levels of cadmium resulted in decreased phosphorylation of c-Jun N-terminal kinase (JNK1/2) in adapted cells than in sensitive cells and this cadmium-induced JNK activity was blocked by JNK inhibitor II, SP600125. Ro318220, a strong activator of JNK, reverted cadmium-sensitive phenotype in adapted cells. Taken together, our results suggest that during cadmium adaptation, cells develop tolerance to cell death, generally due to perturbation of the JNK signaling pathway and the nonresponsiveness of JNK phosphorylation is critical for the Cd-tolerance in these cells.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap-
dc.relation.ispartofToxicology and Applied Pharmacology-
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in [Journal title]. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in PUBLICATION, [VOL#, ISSUE#, (DATE)] DOI#-
dc.subject.meshAdaptation, Physiological-
dc.subject.meshCadmium - toxicity-
dc.subject.meshJNK Mitogen-Activated Protein Kinases - antagonists & inhibitors - metabolism-
dc.subject.meshLung - cytology - drug effects-
dc.subject.meshMetallothionein - genetics - metabolism-
dc.titleAcquired tolerance in cadmium-adapted lung epithelial cells: Roles of the c-Jun N-terminal kinase signaling pathway and basal level of metallothionein-
dc.typeArticle-
dc.identifier.emailLau, TY: andytylau@hotmail.com-
dc.identifier.emailChiu, JF: jfchiu@hkucc.hku.hk-
dc.identifier.doi10.1016/j.taap.2006.01.011-
dc.identifier.pmid16516943-
dc.identifier.scopuseid_2-s2.0-33746359671-
dc.identifier.hkuros120606-
dc.identifier.volume215-
dc.identifier.issue1-
dc.identifier.spage1-
dc.identifier.epage8-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats