Journal
ENVIRONMENTAL TOXICOLOGY
Volume 35, Issue 12, Pages 1334-1342Publisher
WILEY
DOI: 10.1002/tox.22998
Keywords
apoptosis; cadmium; kidney; miR-122-5p; miR-326-3p; PLD1
Categories
Funding
- National Natural Science Foundation of China [81671860]
- Natural Science Foundation of Guangdong Province, China [2018A030313217]
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Cadmium is a toxic heavy metal distributed broadly in the environment and manufactory industry. Long-term exposure to cadmium, considered as a risk for kidney injury, leads to chronic kidney disease eventually. Phospholipase D1 (PLD1) promotes cell proliferation and inhibits apoptosis, and might be involved in cadmium-induced kidney injury. In this study, we used miRNA microarray assays and bioinformatics analysis to identify miRNAs, which may regulate PLD1 expression and exert an impact on cadmium-induced kidney injury. MiR-122-5p and miR-326-3p?selected as candidates, were explored for their regulatory functions in kidney injury, using NRK-52E cells. Both of these two miRNAs exhibited higher expression in kidneys of SD rats after exposure to cadmium for 6 weeks. Cadmium treatment also increased miR-122-5p and miR-326-3p and decreased PLD1 in NRK-52E cells. Both of miR-122-5p and miR-326-3p could downregulate PLD1 expression through targeting its 3 ' UTR and enhance cadmium-induced apoptosis, while inhibiting either of these two miRNAs could reverse such effects. In conclusion, our results suggest that miR-122-5p and miR-326-3p might enhance cadmium-induced NRK-52E cell apoptosis through downregulating PLD1 expression.
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