Oncotarget

Research Papers: Immunology:

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

Yi Yang, Jie Xu, Huo Chen, Xia Fei, YuXu Tang, Yunqiu Yan, Huimin Zhang and Jinping Zhang _

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Oncotarget. 2016; 7:17520-17531. https://doi.org/10.18632/oncotarget.8161

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Abstract

Yi Yang1,*, Jie Xu1,*, Huo Chen1, Xia Fei1, YuXu Tang1, Yunqiu Yan1, Huimin Zhang1 and Jinping Zhang1

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.


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