PUBLICATION

Whole-transcriptome sequencing (RNA-seq) study of the ZFL zebrafish liver cell line after acute exposure to Cd2+ ions

Authors
Kwok, M.L., Meng, Q., Hu, X.L., Chung, C.T., Chan, K.M.
ID
ZDB-PUB-201002-153
Date
2020
Source
Aquatic toxicology (Amsterdam, Netherlands)   228: 105628 (Journal)
Registered Authors
Chan, King-Ming
Keywords
Cadmium, Gene ontology, KEGG, RNA-Seq
MeSH Terms
  • Animals
  • Apoptosis/drug effects
  • Apoptosis/genetics
  • Cadmium/toxicity*
  • Cell Cycle/drug effects
  • Cell Line
  • Endoplasmic Reticulum/drug effects
  • Endoplasmic Reticulum/metabolism
  • Environmental Exposure/analysis*
  • Gene Expression Profiling
  • Gene Expression Regulation/drug effects
  • Gene Ontology
  • Hepatocytes/drug effects
  • Ions
  • Liver/cytology*
  • Liver/drug effects
  • Oxidative Stress/drug effects
  • RNA-Seq*
  • Transcriptome/drug effects
  • Transcriptome/genetics*
  • Water Pollutants, Chemical/toxicity
  • Zebrafish/genetics*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
32971353 Full text @ Aquat. Toxicol.
Abstract
Cadmium (Cd) is a non-essential metal with no known biological function and a broad range of toxic effects in biological systems. We used whole-transcriptome sequencing (RNA-seq) to study the effects of Cd2+ toxicity in zebrafish liver cells, ZFL. The results of an RNA-Seq analysis of ZFL cells exposed to 5, 10 or 20 μM Cd2+ for 4- or 24-h. The differentially expressed genes affected by Cd2+ were analyzed by using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis to study the regulated pathways. Cd2+ regulated the expression of genes associated with cellular Cu, Zn, and Fe homeostasis, DNA replication leading to cell cycle arrest and apoptosis, and glutathione metabolism. Cd2+ boosted up the amino acid synthesis, possibly to support the glutathione metabolism for tackling the oxidative stress generated from Cd2+. Cd2+ stimulation was similar to heat or xenobiotics, based on the responses from ZFL such as endoplasmic reticulum stress and protein folding. We linked also those finding of gene activations relating to carcinogenesis of Cd. This paper provides a comprehensive analysis of the expression profiles induced by Cd2+ exposure in ZFL cells, as well as useful insights into the specific toxic effects.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping