According to an animal study, exposure to e-cigarette aerosol during pregnancy may exacerbate neonatal ischemic brain injury. The underlying process may involve the disruption of the miR-30c-5p and Neurod1 regulatory axis.
Preprint (has not yet undergone peer review). The study investigated how prenatal e-cigarette exposure affects the risk of neonatal ischemic stroke. During the experiment, pregnant rats were exposed to e-cigarette aerosol between embryonic days 4 and 20. Molecular and cellular analyses were conducted on male offspring on postnatal day 10, and brain damage was assessed using a transient middle cerebral artery occlusion (tMCAO) model.
Based on the results, fetal exposure increased infarct size following ischemia, enhanced cell death and aging-related changes, while decreasing markers of neurogenesis and synaptic development. The researchers observed elevated levels of miR-30c-5p and reduced levels of Neurod1 mRNA and protein. Inhibition of miR-30c-5p restored Neurod1 expression, reduced tissue necrosis, and alleviated pathological changes.
The authors highlight that the data suggest an increased sensitivity of the developing brain following e-cigarette exposure; however, a limitation of the results is that the studies were performed exclusively on male rodents.
In Brief
- Preprint publication: the findings have not yet undergone independent peer review.
- Exposure to e-cigarettes during pregnancy increased the extent of ischemic brain injury in male rat offspring.
- The process was associated with the disruption of the miR-30c-5p-Neurod1 regulatory axis, increased apoptosis, and reduced neurogenesis.
- Targeted inhibition of miR-30c-5p was able to mitigate the resulting brain tissue damage.
Source: Europe PMC (doi.org)
This summary was created by artificial intelligence based on the original article.