Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.

<h4>Aim</h4>Iron deficiency is a common comorbidity in chronic heart failure (CHF) which may exacerbate CHF. The c-kit⁺ cardiac stem cells (CSCs) play a vital role in cardiac function repair. However, much is unknown regarding the role of iron deficiency in regulating c-kit⁺ CSCs functio...

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Autores principales:	Dongqiang Song, Yuanmin Li, Jiatian Cao, Zhihua Han, Lin Gao, Zuojun Xu, Zhaofang Yin, Guifang Wang, Yuqi Fan, Changqian Wang
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f10dcc92ed8a4158931bbc527e330f3d
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spelling	oai:doaj.org-article:f10dcc92ed8a4158931bbc527e330f3d2021-11-18T07:42:28ZEffect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.1932-620310.1371/journal.pone.0065721https://doaj.org/article/f10dcc92ed8a4158931bbc527e330f3d2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23762416/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Aim</h4>Iron deficiency is a common comorbidity in chronic heart failure (CHF) which may exacerbate CHF. The c-kit⁺ cardiac stem cells (CSCs) play a vital role in cardiac function repair. However, much is unknown regarding the role of iron deficiency in regulating c-kit⁺ CSCs function. In this study, we investigated whether iron deficiency regulates c-kit⁺ CSCs proliferation, migration, apoptosis, and differentiation in vitro.<h4>Method</h4>All c-kit⁺ CSCs were isolated from adult C57BL/6 mice. The c-kit⁺ CSCs were cultured with deferoxamine (DFO, an iron chelator), mimosine (MIM, another iron chelator), or a complex of DFO and iron (Fe(III)), respectively. Cell migration was assayed using a 48-well chamber system. Proliferation, cell cycle, and apoptosis of c-kit⁺ CSCs were analyzed with BrdU labeling, population doubling time assay, CCK-8 assay, and flow cytometry. Caspase-3 protein level and activity were examined with Western blotting and spectrophotometric detection. The changes in the expression of cardiac-specific proteins (GATA-4,TNI, and β-MHC) and cell cycle-related proteins (cyclin D1, RB, and pRB) were detected with Western blotting.<h4>Result</h4>DFO and MIM suppressed c-kit⁺ CSCs proliferation and differentiation. They also modulated cell cycle and cardiac-specific protein expression. Iron chelators down-regulated the expression and phosphorylation of cell cycle-related proteins. Iron reversed those suppressive effects of DFO. DFO and MIM didn't affect c-kit⁺ CSCs migration and apoptosis.<h4>Conclusion</h4>Iron deficiency suppressed proliferation and differentiation of c-kit⁺ CSCs. This may partly explain how iron deficiency affects CHF prognosis.Dongqiang SongYuanmin LiJiatian CaoZhihua HanLin GaoZuojun XuZhaofang YinGuifang WangYuqi FanChangqian WangPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 6, p e65721 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Dongqiang Song Yuanmin Li Jiatian Cao Zhihua Han Lin Gao Zuojun Xu Zhaofang Yin Guifang Wang Yuqi Fan Changqian Wang Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.
description	<h4>Aim</h4>Iron deficiency is a common comorbidity in chronic heart failure (CHF) which may exacerbate CHF. The c-kit⁺ cardiac stem cells (CSCs) play a vital role in cardiac function repair. However, much is unknown regarding the role of iron deficiency in regulating c-kit⁺ CSCs function. In this study, we investigated whether iron deficiency regulates c-kit⁺ CSCs proliferation, migration, apoptosis, and differentiation in vitro.<h4>Method</h4>All c-kit⁺ CSCs were isolated from adult C57BL/6 mice. The c-kit⁺ CSCs were cultured with deferoxamine (DFO, an iron chelator), mimosine (MIM, another iron chelator), or a complex of DFO and iron (Fe(III)), respectively. Cell migration was assayed using a 48-well chamber system. Proliferation, cell cycle, and apoptosis of c-kit⁺ CSCs were analyzed with BrdU labeling, population doubling time assay, CCK-8 assay, and flow cytometry. Caspase-3 protein level and activity were examined with Western blotting and spectrophotometric detection. The changes in the expression of cardiac-specific proteins (GATA-4,TNI, and β-MHC) and cell cycle-related proteins (cyclin D1, RB, and pRB) were detected with Western blotting.<h4>Result</h4>DFO and MIM suppressed c-kit⁺ CSCs proliferation and differentiation. They also modulated cell cycle and cardiac-specific protein expression. Iron chelators down-regulated the expression and phosphorylation of cell cycle-related proteins. Iron reversed those suppressive effects of DFO. DFO and MIM didn't affect c-kit⁺ CSCs migration and apoptosis.<h4>Conclusion</h4>Iron deficiency suppressed proliferation and differentiation of c-kit⁺ CSCs. This may partly explain how iron deficiency affects CHF prognosis.
format	article
author	Dongqiang Song Yuanmin Li Jiatian Cao Zhihua Han Lin Gao Zuojun Xu Zhaofang Yin Guifang Wang Yuqi Fan Changqian Wang
author_facet	Dongqiang Song Yuanmin Li Jiatian Cao Zhihua Han Lin Gao Zuojun Xu Zhaofang Yin Guifang Wang Yuqi Fan Changqian Wang
author_sort	Dongqiang Song
title	Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.
title_short	Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.
title_full	Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.
title_fullStr	Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.
title_full_unstemmed	Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.
title_sort	effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/f10dcc92ed8a4158931bbc527e330f3d
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Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.

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