Smoking induces differential miRNA expression in human spermatozoa: a potential transgenerational epigenetic concern?

Epigenetics. 2012 May;7(5):432-9. doi: 10.4161/epi.19794. Epub 2012 May 1.


Recent work has suggested that environmental chemicals, including those contained in cigarette smoke, can have adverse effects on the exposed individuals as well as their future progeny. The mechanisms underlying transmission of environmentally induced phenotypes through the germ line are not well understood. However, a predominant process appears to be the establishment of permanent heritable epigenetic alterations, and a number of studies have implicated microRNAs in such processes. Here, we show that cigarette smoke induces specific differences in the spermatozoal microRNA content of human smokers compared with non-smokers, and that these altered microRNAs appear to predominantly mediate pathways vital for healthy sperm and normal embryo development, particularly cell death and apoptosis. microRNA-mediated perturbation of such pathways may explain how harmful phenotypes can be induced in the progeny of smokers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Death
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Environmental Exposure / adverse effects
  • Epigenesis, Genetic*
  • Humans
  • Male
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Oligonucleotide Array Sequence Analysis
  • Smoking / adverse effects*
  • Sperm Count
  • Sperm Motility
  • Spermatozoa / cytology*
  • Spermatozoa / metabolism
  • Tobacco Smoke Pollution / adverse effects
  • Transcription Factor TFIIA / genetics
  • Transcription Factor TFIIA / metabolism
  • Tripartite Motif Proteins
  • Ubiquitin-Protein Ligases
  • Young Adult


  • DNA-Binding Proteins
  • MicroRNAs
  • STON1-GTF2A1L protein, human
  • Tobacco Smoke Pollution
  • Transcription Factor TFIIA
  • Tripartite Motif Proteins
  • TRIM26 protein, human
  • Ubiquitin-Protein Ligases