膜铁转运蛋白的缺失对破骨细胞分化的影响  

Effect of ferroportin deficiency in myeloid lineage cells on osteoclast differentiation

作　　者：周剑[1] 王磊[1] 储彬 Zhou Jian;Wang Lei;Chu Bin(Dept of Orthopedics,The First Affiliated Hospital of Anhui Medical University,Hefei 230022)

机构地区：[1]安徽医科大学第一附属医院骨科,合肥230022

出　　处：《安徽医科大学学报》2018年第12期1893-1897,共5页Acta Universitatis Medicinalis Anhui

基　　金：国家自然科学基金青年基金(编号:81501843)

摘　　要：目的探究在骨髓谱系细胞中特异性敲除膜铁转运蛋白(Fpn)对破骨细胞分化的影响。方法实验组为Fpn基因敲除小鼠,对照组为含Fpn基因的小鼠,分别对两组小鼠骨髓巨噬细胞进行培养并诱导其分化成破骨细胞,且分为巨噬细胞组、前体细胞组、破骨细胞组。通过TRAc P染色、RT-PCR及Western blot等方法探讨Fpn的缺失对破骨细胞分化的影响。结果染色显示实验组中成熟破骨细胞的阳性表达强于对照组。实验组NFATc1、PGC-1β的mRNA表达量及CTSK、NFATc1、PGC-1β的蛋白表达量均高于对照组(P<0. 01)。结论在骨髓谱系细胞中膜铁转运蛋白的缺失会促进破骨细胞的形成。Objective To elucidate the effect of deletion of ferroportin in osteoclast lineage cells on osteoclast differentiation.Methods The Fpn-flox/flox;Cre/+mice were designated as myeloid(FpnΔLysM)Fpn knockout mice.The Fpn-+/+;Cre/+littermates were used as controls.The macrophages from both knockout mice and controls were culture with RANKL and M-CSF,then TRAP staining,RT-PCR and Western blot were used to detect the difference between two strains.Results There was a significant increase in osteoclast formation in Fpn-depleting BMM cultures compared to controls from TRAP staining.The accelerated osteoclastogenesis in Fpn-null BMMs was further confirmed by a higher mRNA expression of osteoclast marker genes,NFATc1 and PGC-1β,in Fpn-null osteoclast lineage cells than in control ones(P<0.01).Similarly,loss of FPN resulted in elevation of protein levels of CTSK,NFATc1,and PGC-1βin the course of osteoclast differentiation.Conclusion FPN deficiency in myeloid lineage cells stimulates osteoclastogenesis in vitro.

关 键 词：膜铁转运蛋白 破骨细胞 分化 

分 类 号：R681[医药卫生—骨科学]