MiR-128-2 inhibits common lymphoid progenitors from developing into progenitor B cells

// Yi Yang 1,* , Jie Xu 1,* , Huo Chen 1 , Xia Fei 1 , YuXu Tang 1 , Yunqiu Yan 1 , Huimin Zhang 1 and Jinping Zhang 1 1 Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province, People’s Republic of China * These authors have contributed equally to this work Correspondence to: Jinping Zhang, email: // Huimin Zhang, email: // Keywords : miR-128-2, CLP, B cell development, apoptosis, Immunology and Microbiology Section, Immune response, Immunity Received : January 14, 2016 Accepted : March 04, 2016 Published : March 17, 2016 Abstract 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.