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Perinatal Exposure to Nicotine Alters Sperm RNA Profiles in Rats
Hetan Wang1,2, Jie Liu2, Jianjun Gao2
1Department of Medical Genetics, China Medical University, Shenyang, China.
Insights
Perinatal nicotine exposure alters sperm RNA profiles, potentially contributing to heritable asthma. A PPARγ agonist, rosiglitazone, reversed these epigenetic changes in offspring.
Area of Science:
- Epigenetics
- Developmental Toxicology
- Pediatric Asthma
Background:
- Childhood asthma is a common pediatric condition with a suspected heritable component.
- Perinatal smoking exposure is linked to asthma, but molecular mechanisms remain unclear.
- Epigenetic inheritance is a proposed mechanism, supported by prior DNA methylation and histone acetylation data.
Purpose of the Study:
- To investigate the epigenetic inheritance of asthma induced by perinatal nicotine exposure.
- To profile large and small RNAs in the sperm of F1 male rats exposed perinatally to nicotine.
Main Methods:
- Profiling of large and small RNAs in sperm from F1 male rats.
- Analysis of RNA alterations following perinatal nicotine exposure.
- Assessment of rosiglitazone's effect on nicotine-induced RNA changes.
Main Results:
- Perinatal nicotine exposure altered sperm-borne RNA profiles (mRNAs and small RNAs).
- Rosiglitazone, a PPARγ agonist, attenuated nicotine's effects.
- Rosiglitazone reversed sperm-borne RNA profiles toward placebo control levels.
Conclusions:
- Perinatal nicotine exposure induces epigenetic changes in sperm RNA profiles.
- These RNA alterations may mediate the transgenerational inheritance of asthma.
- PPARγ agonism offers a potential therapeutic strategy to counteract these effects.
Abstract:
Perinatal exposure to smoking has been associated with childhood asthma, one of the most common pediatric conditions affecting millions of children globally. Of great interest, this disease phenotype appears heritable as it can persist across multiple generations even in the absence of persistent exposure to smoking in subsequent generations. Although the molecular mechanisms underlying childhood asthma induced by perinatal exposure to smoking or nicotine remain elusive, an epigenetic mechanism has been proposed, which is supported by the data from our earlier analyses on germline DNA methylation (5mC) and histone marks (H3 and H4 acetylation). To further investigate the potential epigenetic inheritance of childhood asthma induced by perinatal nicotine exposure, we profiled both large and small RNAs in the sperm of F1 male rats. Our data revealed that perinatal exposure to nicotine leads to alterations in the profiles of sperm-borne RNAs, including mRNAs and small RNAs, and that rosiglitazone, a PPARγ agonist, can attenuate the effect of nicotine and reverse the sperm-borne RNA profiles of F1 male rats to close to placebo control levels.
