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Article: Deferiprone inhibits iron overload-induced tissue factor bearing endothelial microparticle generation by inhibition oxidative stress induced mitochondrial injury, and apoptosis

TitleDeferiprone inhibits iron overload-induced tissue factor bearing endothelial microparticle generation by inhibition oxidative stress induced mitochondrial injury, and apoptosis
Authors
KeywordsApoptosis
Endothelial microparticles
Iron
L1
Mitochondria
Issue Date2018
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap
Citation
Toxicology and Applied Pharmacology, 2018, v. 338, p. 148-158 How to Cite?
AbstractIron overload-induced cardiovascular toxicity is one of the most common causes of morbidity and mortality in beta-thalassemia major patients. We have previously shown that iron overload-induced systemic arterial changes characterized by endothelial dysfunction are associated with increased endothelial microparticle (EMP) release. In this study, we further demonstrate how EMP release is associated with iron-induced mitochondrial injury and apoptosis of endothelial cells. Iron increased the production of reactive oxygen species (ROS) and calcium influx into mitochondria [Ca2+]m. Iron also disturbed mitochondrial respiration function and eventually led to loss of mitochondrial membrane potential (ΔΨm). A significant increase in apoptotic cells and EMPs were found under iron treatment. EMPs contained tissue factor (TF), which has potential clinical impact on thromboembolic phenomenon. Then, we investigated the salvaging effect of deferiprone (L1) on endothelial cell damage and EMP release. We found that L1 could inhibit iron-induced ROS generation, and decrease mitochondrial damage with the resultant effect of less endothelial cell apoptosis and EMP release. L1 could protect endothelial cells from iron-induced toxic effects and minimize EMP release, which could be potentially helpful in a subgroup of thalassemia patients who have increased thromboembolic complications.
Persistent Identifierhttp://hdl.handle.net/10722/251861
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 0.788
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, S-
dc.contributor.authorLian, Q-
dc.contributor.authorChen, MP-
dc.contributor.authorJiang, D-
dc.contributor.authorHo, JTK-
dc.contributor.authorCheung, YF-
dc.contributor.authorChan, GCF-
dc.date.accessioned2018-03-21T07:30:28Z-
dc.date.available2018-03-21T07:30:28Z-
dc.date.issued2018-
dc.identifier.citationToxicology and Applied Pharmacology, 2018, v. 338, p. 148-158-
dc.identifier.issn0041-008X-
dc.identifier.urihttp://hdl.handle.net/10722/251861-
dc.description.abstractIron overload-induced cardiovascular toxicity is one of the most common causes of morbidity and mortality in beta-thalassemia major patients. We have previously shown that iron overload-induced systemic arterial changes characterized by endothelial dysfunction are associated with increased endothelial microparticle (EMP) release. In this study, we further demonstrate how EMP release is associated with iron-induced mitochondrial injury and apoptosis of endothelial cells. Iron increased the production of reactive oxygen species (ROS) and calcium influx into mitochondria [Ca2+]m. Iron also disturbed mitochondrial respiration function and eventually led to loss of mitochondrial membrane potential (ΔΨm). A significant increase in apoptotic cells and EMPs were found under iron treatment. EMPs contained tissue factor (TF), which has potential clinical impact on thromboembolic phenomenon. Then, we investigated the salvaging effect of deferiprone (L1) on endothelial cell damage and EMP release. We found that L1 could inhibit iron-induced ROS generation, and decrease mitochondrial damage with the resultant effect of less endothelial cell apoptosis and EMP release. L1 could protect endothelial cells from iron-induced toxic effects and minimize EMP release, which could be potentially helpful in a subgroup of thalassemia patients who have increased thromboembolic complications.-
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.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subjectApoptosis-
dc.subjectEndothelial microparticles-
dc.subjectIron-
dc.subjectL1-
dc.subjectMitochondria-
dc.titleDeferiprone inhibits iron overload-induced tissue factor bearing endothelial microparticle generation by inhibition oxidative stress induced mitochondrial injury, and apoptosis-
dc.typeArticle-
dc.identifier.emailChan, S: schan88@hkucc.hku.hk-
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hk-
dc.identifier.emailCheung, YF: xfcheung@hku.hk-
dc.identifier.emailChan, GCF: gcfchan@hku.hk-
dc.identifier.authorityLian, Q=rp00267-
dc.identifier.authorityCheung, YF=rp00382-
dc.identifier.authorityChan, GCF=rp00431-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.taap.2017.11.005-
dc.identifier.pmid29132816-
dc.identifier.scopuseid_2-s2.0-85037076884-
dc.identifier.hkuros287511-
dc.identifier.hkuros295346-
dc.identifier.volume338-
dc.identifier.spage148-
dc.identifier.epage158-
dc.identifier.isiWOS:000422894200015-
dc.publisher.placeUnited States-
dc.identifier.issnl0041-008X-

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