当前位置: X-MOL 学术Mol. Biol. Rep. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Relation of hepcidin gene expression in blood mononuclear cells with iron overload severity among β-thalassemia major patients
Molecular Biology Reports ( IF 2.8 ) Pub Date : 2020-11-24 , DOI: 10.1007/s11033-020-06012-2
Hossein Ayatollahi , Seyedeh Fatemeh Mousavi Nezhad , Amir Talebpour , Zahra Badiei , Hossein Nezami

Iron overload is the main cause of morbidity and mortality in β-thalassemia major patients, and cardiac iron overload is the most common reason for death in these transfusion-dependent patients. Hepcidin, a liver-derived peptide hormone, plays a key role in plasma iron levels regulation by controlling two main stages, digestive iron absorption in enterocytes, and iron recycling in macrophages. Although hepcidin is mainly secreted from hepatocytes in the liver, it is also synthesized from mononuclear cells consisting of monocytes and lymphocytes. Binding of this molecule to ferroportin, a specific cellular exporter of iron, leads to degradation of the ligand-receptor complex, which reduces the iron overload by lowering the amounts of iron released into the plasma. Likewise, the same mechanism has been proved to be true for lymphocyte-drived hepcidin. The expression levels of hepcidin mRNA were evaluated using quantitative real time PCR (qRT-PCR) in 50 β-thalassemia major patients, as well as 25 healthy volunteers as the group of control. There was a significantly positive correlation between the cardiac iron concentration, showed by higher T2 values, and hepcidin levels in the patients (p = 0.028; r = 0.311). However, hepcidin expression levels did not significantly correlate with ferritin and liver iron concentrations. Hepcidin can act as a beneficial marker to determine iron overload degrees, particularly in the heart, in β-thalassemia major patients and be used as a logical therapeutic agent for treatment of β-thalassemia disorders.



中文翻译:

重型β地中海贫血患者血液单核细胞中铁调素基因表达与铁超载严重程度的关系

铁超负荷是严重β-地中海贫血患者发病和死亡的主要原因,而心脏铁超负荷是这些依赖输血的患者死亡的最常见原因。Hepcidin是一种肝脏衍生的肽激素,它通过控制两个主要阶段(肠细胞中的消化铁吸收和巨噬细胞中的铁回收)来控制血浆铁水平。尽管铁调素主要从肝脏的肝细胞分泌,但它也由单核细胞和淋巴细胞组成的单核细胞合成。该分子与铁转运蛋白(铁的特定细胞输出物)结合导致配体-受体复合物降解,从而通过降低释放到血浆中的铁量来减少铁超载。同样 事实证明,淋巴细胞驱动的铁调素具有相同的机制。使用定量实时PCR(qRT-PCR)评估了50名重型地中海贫血患者以及25名健康志愿者(作为对照组)中hepcidin mRNA的表达水平。T2值较高表明患者的心脏铁浓度与铁调素水平之间存在显着正相关(p = 0.028; r = 0.311)。但是,铁调素的表达水平与铁蛋白和肝铁浓度没有显着相关。铁调素可以作为确定β地中海贫血重症患者尤其是心脏中铁超负荷程度的有益标志物,并可以用作治疗β地中海贫血疾病的合理治疗剂。使用定量实时PCR(qRT-PCR)评估了50名重型地中海贫血患者以及25名健康志愿者(作为对照组)中hepcidin mRNA的表达水平。T2值较高表明患者的心脏铁浓度与铁调素水平之间存在显着正相关(p = 0.028; r = 0.311)。但是,铁调素的表达水平与铁蛋白和肝铁浓度没有显着相关。铁调素可以作为确定β地中海贫血重症患者尤其是心脏中铁超负荷程度的有益标志物,并可以用作治疗β地中海贫血疾病的合理治疗剂。使用定量实时PCR(qRT-PCR)评价了50名地中海贫血重症患者以及对照组的25名健康志愿者中hepcidin mRNA的表达水平。T2值较高表明患者的心脏铁浓度与铁调素水平之间存在显着正相关(p = 0.028; r = 0.311)。但是,铁调素的表达水平与铁蛋白和肝铁浓度没有显着相关。铁调素可以作为确定β地中海贫血重症患者尤其是心脏中铁超负荷程度的有益标志物,并可以用作治疗β地中海贫血疾病的合理治疗剂。T2值较高表明患者的心脏铁浓度与铁调素水平之间存在显着正相关(p = 0.028; r = 0.311)。但是,铁调素的表达水平与铁蛋白和肝铁浓度没有显着相关。铁调素可以作为确定β地中海贫血重症患者尤其是心脏中铁超负荷程度的有益标志物,并可以用作治疗β地中海贫血疾病的合理治疗剂。T2值较高表明患者的心脏铁浓度与铁调素水平之间存在显着正相关(p = 0.028; r = 0.311)。但是,铁调素的表达水平与铁蛋白和肝铁浓度没有显着相关。铁调素可以作为确定β地中海贫血重症患者尤其是心脏中铁超负荷程度的有益标志物,并可以用作治疗β地中海贫血疾病的合理治疗剂。

更新日期:2020-11-25
down
wechat
bug