miR-150 inhibits terminal erythroid proliferation and differentiation
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Zhiwei Sun1, Ye Wang1, Xu Han1, Xielan Zhao2, Yuanliang Peng1, Yusheng Li2, Minyuan Peng2, Jianhui Song2, Kunlu Wu1, Shumin Sun1, Weihua Zhou1, Biwei Qi1, Chufan Zhou1, Huiyong Chen1, Xiuli An3,4, Jing Liu1
1The State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China
2Xiangya Hospital, Central South University, Changsha 410008, China
3College of Life Sciences, Zhengzhou University, Zhengzhou 450001, China
4Laboratory of Membrane Biology, New York Blood Center, New York, NY 10065, USA
Jing Liu, e-mail: [email protected]
Xiuli An, e-mail: [email protected]
Huiyong Chen, e-mail: [email protected]
Keywords: miR-150, terminal erythropoiesis, 4.1R, erythroid proliferation, transcriptional profiling
Received: May 15, 2015 Accepted: October 22, 2015 Published: November 03, 2015
MicroRNAs (miRNAs), a class of small non-coding linear RNAs, have been shown to play a crucial role in erythropoiesis. To evaluate the indispensable role of constant suppression of miR-150 during terminal erythropoiesis, we performed miR-150 gain- and loss-of-function experiments on hemin-induced K562 cells and EPO-induced human CD34+ cells. We found that forced expression of miR-150 suppresses commitment of hemoglobinization and CD235a labeling in both cell types. Erythroid proliferation is also inhibited via inducing apoptosis and blocking the cell cycle when miR-150 is overexpressed. In contrast, miR-150 inhibition promotes terminal erythropoiesis. 4.1 R gene is a new target of miR-150 during terminal erythropoiesis, and its abundance ensures the mechanical stability and deformability of the membrane. However, knockdown of 4.1 R did not affect terminal erythropoiesis. Transcriptional profiling identified more molecules involved in terminal erythroid dysregulation derived from miR-150 overexpression. These results shed light on the role of miR-150 during human terminal erythropoiesis. This is the first report highlighting the relationship between miRNA and membrane protein and enhancing our understanding of how miRNA works in the hematopoietic system.
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