PUBLICATION

miR-21 is involved in skeletal deficiencies of zebrafish embryos exposed to polychlorinated biphenyls

Authors
Ju, L., Zhou, Z., Jiang, B., Lou, Y., Zhang, Z.
ID
ZDB-PUB-161025-26
Date
2017
Source
Environmental science and pollution research international   24(1): 886-891 (Journal)
Registered Authors
Keywords
BMPRII, Biphenyls, Calcium, Embryonic development, Skeletal deficiency, Zebrafish, miR-21
MeSH Terms
  • Animals
  • Bone Diseases, Developmental/chemically induced*
  • Bone Diseases, Developmental/embryology
  • Bone Diseases, Developmental/metabolism
  • Bone Diseases, Developmental/pathology
  • Bone Morphogenetic Protein Receptors, Type II/genetics
  • Calcium/metabolism
  • Embryo, Nonmammalian/abnormalities
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/metabolism
  • Embryo, Nonmammalian/pathology
  • Embryonic Development/drug effects
  • Embryonic Development/genetics
  • MicroRNAs/genetics*
  • Polychlorinated Biphenyls/toxicity*
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish*/embryology
  • Zebrafish Proteins/genetics
PubMed
27761858 Full text @ Environ. Sci. Pollut. Res. Int.
Abstract
Polychlorinated biphenyl (PCB) exposure increases the incidence and severity of skeletal diseases, but little is known about the mechanisms that mediate this relationship. We exposed zebrafish embryos to PCB1254 and assessed the changes in bone morphology protein receptor II (BMPRII), which is involved in bone formation and embryonic development, miRNA-21, for which BMPRII is a known target, and calcium metabolism. PCB1254 upregulated the expression of miR-21 and suppressed BMPRII expression. The inhibition of miR-21 reversed the downregulation of BMPRII and alleviated the PCB1254-induced loss of calcium. These findings suggest new biomarkers of developmental defects of the skeleton caused by PCBs.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping