PUBLICATION

Inducible overexpression of zebrafish microRNA-722 suppresses chemotaxis of human neutrophil like cells

Authors
Hsu, A.Y., Liu, S., Syahirah, R., Brasseale, K.A., Wan, J., Deng, Q.
ID
ZDB-PUB-190609-5
Date
2019
Source
Molecular immunology   112: 206-214 (Journal)
Registered Authors
Deng, Qing, Hsu, Alan
Keywords
Chemotaxis, HL-60, Inducible expression, RAC2, Signaling, microRNA
MeSH Terms
  • Actins/genetics
  • Animals
  • Cell Differentiation/genetics
  • Cell Line
  • Cell Line, Tumor
  • Cell Movement/genetics
  • Chemotaxis/genetics*
  • HEK293 Cells
  • HL-60 Cells
  • Humans
  • Inflammation/genetics
  • Leukemia/genetics
  • MicroRNAs/genetics*
  • Neutrophils/physiology*
  • RNA, Messenger/genetics
  • Reactive Oxygen Species/metabolism
  • Signal Transduction/genetics
  • Zebrafish/genetics*
  • Zebrafish Proteins/genetics
  • rac GTP-Binding Proteins/genetics
PubMed
31176200 Full text @ Mol. Immunol.
Abstract
Neutrophil migration is essential for battling against infections but also drives chronic inflammation. Since primary neutrophils are terminally differentiated and not genetically tractable, leukemia cells such as HL-60 are differentiated into neutrophil-like cells to study mechanisms underlying neutrophil migration. However, constitutive overexpression or inhibition in this cell line does not allow the characterization of the genes that affect the differentiation process. Here we apply the tet-on system to induce the expression of a zebrafish microRNA, dre-miR-722, in differentiated HL-60. Overexpression of miR-722 reduced the mRNA level of genes in the chemotaxis and inflammation pathways, including Ras-Related C3 Botulinum Toxin Substrate 2 (RAC2). Consistently, polarization of the actin cytoskeleton, cell migration and generation of the reactive oxygen species are significantly inhibited upon induced miR-722 overexpression. Together, zebrafish miR-722 is a suppressor for migration and signaling in human neutrophil like cells.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping