Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels

Iron-overload cardiomyopathy is a major cause of death in thalassemic patients. However, pathways of non-transferrin-bound iron (NTBI) uptake into cardiomyocytes under iron-overload conditions are still controversial. We previously demonstrated that Fe2+ uptake in thalassemic cardiomyocytes is mainl...

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Main Authors: Kumfu S., Chattipakorn S., Fucharoen S., Chattipakorn N.
Format: Article
Language:English
Published: 2014
Online Access:http://www.scopus.com/inward/record.url?eid=2-s2.0-84871211904&partnerID=40&md5=321b391f246ccfd69084a4033274c59e
http://cmuir.cmu.ac.th/handle/6653943832/4241
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Institution: Chiang Mai University
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spelling th-cmuir.6653943832-42412014-08-30T02:35:49Z Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels Kumfu S. Chattipakorn S. Fucharoen S. Chattipakorn N. Iron-overload cardiomyopathy is a major cause of death in thalassemic patients. However, pathways of non-transferrin-bound iron (NTBI) uptake into cardiomyocytes under iron-overload conditions are still controversial. We previously demonstrated that Fe2+ uptake in thalassemic cardiomyocytes is mainly mediated by T-type calcium channels (TTCCs). However, direct evidence regarding Fe3+ uptake, the other form of NTBI, in thalassemic cardiomyocytes has never been investigated. Hearts from genetic-altered ?-thalassemic mice and adult wild-type (WT) mice were used for cultured ventricular cardiomyocytes. Blockers for L-type calcium channel (LTCC), TTCC, transferrin receptor1 (TfR1), and divalent metal transporter1 (DMT1) were used, and quantification of cellular iron uptake was performed by the acetoxymethyl ester of calcein fluorescence assay. Cellular uptake of Fe3+ under iron-overload conditions in cultured ventricular myocytes of thalassemic mice was greater than that of WT cells (P < 0.01). The iron chelator, deferoxamine, could prevent Fe3+ uptake into cultured cardiomyocytes. However, blockers of TfR1, DMT1, LTCC, and TTCC could not prevent Fe3+ uptake into cardiomyocytes. Our findings indicated that, unlike Fe2+, Fe3+ uptake in cultured thalassemic cardiomyocytes is not mainly mediated by TfR1, DMT1, LTCC, and TTCC, suggesting that another alternative pathway could play a major role in Fe3+ uptake in thalassemic cardiomyocytes. ? 2013 Informa Healthcare USA, Inc. 2014-08-30T02:35:49Z 2014-08-30T02:35:49Z 2013 Article 1480545 10.3109/01480545.2012.726625 23050671 DCTOD http://www.scopus.com/inward/record.url?eid=2-s2.0-84871211904&partnerID=40&md5=321b391f246ccfd69084a4033274c59e http://cmuir.cmu.ac.th/handle/6653943832/4241 English
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
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language English
description Iron-overload cardiomyopathy is a major cause of death in thalassemic patients. However, pathways of non-transferrin-bound iron (NTBI) uptake into cardiomyocytes under iron-overload conditions are still controversial. We previously demonstrated that Fe2+ uptake in thalassemic cardiomyocytes is mainly mediated by T-type calcium channels (TTCCs). However, direct evidence regarding Fe3+ uptake, the other form of NTBI, in thalassemic cardiomyocytes has never been investigated. Hearts from genetic-altered ?-thalassemic mice and adult wild-type (WT) mice were used for cultured ventricular cardiomyocytes. Blockers for L-type calcium channel (LTCC), TTCC, transferrin receptor1 (TfR1), and divalent metal transporter1 (DMT1) were used, and quantification of cellular iron uptake was performed by the acetoxymethyl ester of calcein fluorescence assay. Cellular uptake of Fe3+ under iron-overload conditions in cultured ventricular myocytes of thalassemic mice was greater than that of WT cells (P < 0.01). The iron chelator, deferoxamine, could prevent Fe3+ uptake into cultured cardiomyocytes. However, blockers of TfR1, DMT1, LTCC, and TTCC could not prevent Fe3+ uptake into cardiomyocytes. Our findings indicated that, unlike Fe2+, Fe3+ uptake in cultured thalassemic cardiomyocytes is not mainly mediated by TfR1, DMT1, LTCC, and TTCC, suggesting that another alternative pathway could play a major role in Fe3+ uptake in thalassemic cardiomyocytes. ? 2013 Informa Healthcare USA, Inc.
format Article
author Kumfu S.
Chattipakorn S.
Fucharoen S.
Chattipakorn N.
spellingShingle Kumfu S.
Chattipakorn S.
Fucharoen S.
Chattipakorn N.
Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels
author_facet Kumfu S.
Chattipakorn S.
Fucharoen S.
Chattipakorn N.
author_sort Kumfu S.
title Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels
title_short Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels
title_full Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels
title_fullStr Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels
title_full_unstemmed Ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels
title_sort ferric iron uptake into cardiomyocytes of ?-thalassemic mice is not through calcium channels
publishDate 2014
url http://www.scopus.com/inward/record.url?eid=2-s2.0-84871211904&partnerID=40&md5=321b391f246ccfd69084a4033274c59e
http://cmuir.cmu.ac.th/handle/6653943832/4241
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