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Article: Aberrant cytokine secretion and zinc uptake in chronic cadmium-exposed lung epithelial cells

TitleAberrant cytokine secretion and zinc uptake in chronic cadmium-exposed lung epithelial cells
Authors
Issue Date2017
Citation
PROTEOMICS - Clinical Applications, 2017, v. 11, p. 1600059 How to Cite?
AbstractPURPOSE: Our previous results showed that cadmium (Cd)-adapted lung epithelial cells (LECs) developed resistance to apoptosis due to non-responsiveness of the c-Jun N-terminal kinase pathway and augmented expression of cytokeratin 8. Since cellular Cd entry is a prerequisite in order for Cd to elicit its cytotoxicity, therefore, we wonder if there are differential metal ion transport ability and also other phenotypic changes that occurred in these Cd-resistant LECs. EXPERIMENTAL DESIGN AND RESULTS: Here, we explored further and found that the zinc (Zn) importer Zip8 was stably abolished in these cells along with a marked decrease of Cd and Zn accumulation. Moreover, by cell migration assays and cytokine antibody array analysis, we found that Cd-adapted cells exhibit enhanced migratory ability possibly due to elevated secretions of vascular endothelial growth factor and macrophage inflammatory protein-3 alpha (MIP-3α). CONCLUSION AND CLINICAL RELEVANCE: Taken together, our results show that during chronic Cd exposure, lung cells antagonize excessive cellular Cd-influx by abolishing Zip8 expression to reduce Cd-toxicity; however, this also renders cells with a diminished Zn uptake. The imbalance of Zn homeostasis and elevation of angiogenic and epithelial-mesenchymal transition-promoting cytokines in Cd-adapted cells might thus likely promote Zn deficiency, angiogenesis, and cell invasion.
Persistent Identifierhttp://hdl.handle.net/10722/246939
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXu, YM-
dc.contributor.authorGao, YM-
dc.contributor.authorWu, DD-
dc.contributor.authorYu, FY-
dc.contributor.authorZang, ZS-
dc.contributor.authorYang, L-
dc.contributor.authorYao, Y-
dc.contributor.authorCai, NL-
dc.contributor.authorZhou, Y-
dc.contributor.authorChiu, JF-
dc.contributor.authorChing, YP-
dc.contributor.authorLau, AT-
dc.date.accessioned2017-10-18T08:19:41Z-
dc.date.available2017-10-18T08:19:41Z-
dc.date.issued2017-
dc.identifier.citationPROTEOMICS - Clinical Applications, 2017, v. 11, p. 1600059-
dc.identifier.urihttp://hdl.handle.net/10722/246939-
dc.description.abstractPURPOSE: Our previous results showed that cadmium (Cd)-adapted lung epithelial cells (LECs) developed resistance to apoptosis due to non-responsiveness of the c-Jun N-terminal kinase pathway and augmented expression of cytokeratin 8. Since cellular Cd entry is a prerequisite in order for Cd to elicit its cytotoxicity, therefore, we wonder if there are differential metal ion transport ability and also other phenotypic changes that occurred in these Cd-resistant LECs. EXPERIMENTAL DESIGN AND RESULTS: Here, we explored further and found that the zinc (Zn) importer Zip8 was stably abolished in these cells along with a marked decrease of Cd and Zn accumulation. Moreover, by cell migration assays and cytokine antibody array analysis, we found that Cd-adapted cells exhibit enhanced migratory ability possibly due to elevated secretions of vascular endothelial growth factor and macrophage inflammatory protein-3 alpha (MIP-3α). CONCLUSION AND CLINICAL RELEVANCE: Taken together, our results show that during chronic Cd exposure, lung cells antagonize excessive cellular Cd-influx by abolishing Zip8 expression to reduce Cd-toxicity; however, this also renders cells with a diminished Zn uptake. The imbalance of Zn homeostasis and elevation of angiogenic and epithelial-mesenchymal transition-promoting cytokines in Cd-adapted cells might thus likely promote Zn deficiency, angiogenesis, and cell invasion.-
dc.languageeng-
dc.relation.ispartofPROTEOMICS - Clinical Applications-
dc.titleAberrant cytokine secretion and zinc uptake in chronic cadmium-exposed lung epithelial cells-
dc.typeArticle-
dc.identifier.emailZhou, Y: yzhou@hku.hk-
dc.identifier.emailChing, YP: ypching@hku.hk-
dc.identifier.authorityChing, YP=rp00469-
dc.identifier.doi10.1002/prca.201600059-
dc.identifier.hkuros282432-
dc.identifier.volume11-
dc.identifier.spage1600059-
dc.identifier.epage1600059-
dc.identifier.isiWOS:000398049000003-

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