miR-142-3p acts as an essential modulator of neutrophil development in zebrafish

Hong Bo Fan, Yi Jie Liu, Lei Wang, Ting Ting Du, Mei Dong, Li Gao, Zhao Zheng Meng, Yi Jin, Yi Chen, Min Deng, Huang Tian Yang, Qing Jing, Ai Hua Gu*, Ting Xi Liu, Yong Zhou

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Neutrophils play critical roles in vertebrate innate immune responses. As an emerging regulator in normal myelopoiesis, the precise roles of microRNA in the development of neutrophils have yet to be clarified. Using zinc-finger nucleases, we have successfully generated heritable mutations in miR-142a and miR-142b and showed that hematopoietic-specific miR-142-3p is completely deleted in miR-142 double mutant zebrafish. The lack of miR-142-3p resulted in aberrant reduction and hypermaturation of neutrophils in definitive myelopoiesis, as well as impaired inflammatory migration of neutrophils in the fetal stage. Furthermore, the adult myelopoiesis in the miR-142-3p-deficient zebrafish was also affected, producing irregular hypermature neutrophils with increased cell size and a decreased nucleocytoplasmic ratio. Additionally, miR-142-3p-deficient zebrafish are expected to develop a chronic failure of myelopoiesis with age. Transcriptome analysis showed an aberrant activation of the interferon γ (IFN-γ) signaling pathway in myelomonocytes after miR-142-3p deletion. We found that the reduced number and hypermaturation of neutrophils caused by loss of miR-142-3p was mainly mediated by the abnormally activated IFN-γ signaling, especially the upregulation of stat1a and irf1b. Taken together, we uncovered a novel role of miR-142-3p in maintaining normal neutrophil development and maturation.

Original languageEnglish (US)
Pages (from-to)1320-1330
Number of pages11
Issue number8
StatePublished - Aug 21 2014

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology


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