MiR-128-2 inhibits common lymphoid progenitors from developing into progenitor B cells.
MiR-128-2 inhibits common lymphoid progenitors from developing into progenitor B cells.
复制标题
MiR-128-2 抑制共同淋巴祖细胞发育成祖 B 细胞
DOI：
10.18632/oncotarget.8161
复制
发表时间：
2016-04-05
期刊：
影响因子：
--
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Yang Y;Xu J;Chen H;Fei X;Tang Y;Yan Y;Zhang H;Zhang J
大量研究表明，B细胞的发育受转录因子（TF）的精细调控。最近的研究表明，TF与microRNA协调，在许多检查点控制B细胞的发育。本研究首次发现miR-128-2在多种免疫器官和免疫细胞中差异表达。在miR-128-2过表达嵌合体和转基因（TG）小鼠中，骨髓中的B细胞发育受到抑制，前原B、前B、前B、未成熟B和再循环B细胞减少，共同淋巴祖细胞（CLP）增加。进一步的实验表明，在miR-128-2过表达的小鼠中，CLP的凋亡减少，但增殖没有改变。大量研究表明，miR-128-2可能通过靶向A2 B和MALT 1，增加ERK和P38 MAPK的磷酸化，从而抑制CLP的凋亡。这些发现促使了对miR-128-2在淋巴发生中的功能的进一步研究。
A considerable number of studies revealed that B cell development is finely regulated by transcription factors (TFs). Recent studies suggested that TFs are coordinated with microRNAs to control the development of B cells in numerous checkpoints. In the present study, we first found that miR-128-2 was differentially expressed in various immune organs and immunocytes. B cell development was inhibited in miR-128-2-overexpressed chimera and transgenic (TG) mice in bone marrow with decreased preproB, preB, proB, immature B, and recirculating B cells, as well as increased common lymphoid progenitors (CLPs). Further experiments showed that the apoptosis of CLP decreased, but proliferation was not altered in miR-128-2-overexpressed mice. Extensive studies suggested that the inhibition of apoptosis of CLP may be caused by miR-128-2 targeting A2B and MALT1, thereby increasing the phosphorylation of ERK and P38 MAPK. Such findings have prompted future investigations on the function of miR-128-2 in lymph genesis.