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Effect of Iron Deficiency on c-kit(+) Cardiac Stem Cells In Vitro

AIM: 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 stud...

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Detalles Bibliográficos
Autores principales: Song, Dongqiang, Li, Yuanmin, Cao, Jiatian, Han, Zhihua, Gao, Lin, Xu, Zuojun, Yin, Zhaofang, Wang, Guifang, Fan, Yuqi, Wang, Changqian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677875/
https://www.ncbi.nlm.nih.gov/pubmed/23762416
http://dx.doi.org/10.1371/journal.pone.0065721
Descripción
Sumario:AIM: 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. METHOD: 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. RESULT: 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. CONCLUSION: Iron deficiency suppressed proliferation and differentiation of c-kit(+) CSCs. This may partly explain how iron deficiency affects CHF prognosis.