ArticleFrontiers in molecular neuroscience2017
Maternal Cigarette Smoke Exposure Worsens Neurological Outcomes in Adolescent Offspring with Hypoxic-Ischemic Injury.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Maternal metformin protects developing auditory brainstem function after neonatal hypoxia-ischemia in a neonatal rat model.Clinical and experimental pediatrics · 2026Article
- Article
- Maternal e-cigarette use can disrupt postnatal blood-brain barrier (BBB) integrity and deteriorates motor, learning and memory function: influence of sex and age.Fluids and barriers of the CNS · 2023Article
- Mitochondrial dysfunction in a rat model and the related risk of metabolic disorders.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Environmental tobacco smoke exposure and non-syndromic orofacial cleft: Systematic review and meta-analysis.Tobacco induced diseases · 2023Review
- Maternal Cigarette Smoke Exposure Exaggerates the Behavioral Defects and Neuronal Loss Caused by Hypoxic-Ischemic Brain Injury in Female Offspring.Frontiers in cellular neuroscience · 2022Article
- Maternal Inflammation Exaggerates Offspring Susceptibility to Cerebral Ischemia-Reperfusion Injury via the COX-2/PGD2/DPOxidative medicine and cellular longevity · 2022Article
- Editorial: Perinatal hypoxic-ischemic brain injury: Mechanisms, pathogenesis, and potential therapeutic strategies.Frontiers in cellular neuroscience · 2022Article
- Fetal e-cigarette exposure programs a neonatal brain hypoxic-ischemic sensitive phenotype via altering DNA methylation patterns and autophagy signaling pathway.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Maternal High Fat Diet Consumption Exaggerates Metabolic Disorders in Mice With Cigarette-Smoking Induced Intrauterine Undernutrition.Frontiers in nutrition · 2021Article
- Neuroinflammatory and Behavioral Outcomes Measured in Adult Offspring of Mice Exposed Prenatally to E-Cigarette Aerosols.Environmental health perspectives · 2020Article
- In Situ Ligand-Directed Growth of Gold Nanoparticles in Biological Tissues.Nano letters · 2020Article
- Cell death in the human infant central nervous system and in sudden infant death syndrome (SIDS).Apoptosis : an international journal on programmed cell death · 2019Article
- L-Carnitine and extendin-4 improve outcomes following moderate brain contusion injury.Scientific reports · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxic-ischemic (HI) encephalopathy occurs in approximately 6 per 1000 term newborns leading to devastating neurological consequences, such as cerebral palsy and seizures. Maternal smoking is one of the prominent risk factors contributing to HI injury. Mitochondrial integrity plays a critical role in neural injury and repair during HI. We previously showed that maternal cigarette smoke exposure (SE) can reduce brain mitochondrial fission and autophagosome markers in male offspring. This was accompanied by increased brain cell apoptosis (active caspase-3) and DNA fragmentation (TUNEL staining). Here, we aimed to investigate whether maternal SE leads to more severe neurological damage after HI brain injury in male offspring. Female BALB/c mice (8 weeks) were exposed to cigarette smoke prior to mating, during gestation, and lactation. At postnatal day 10, half of the pups from each litter underwent left carotid artery occlusion, followed by exposure to 8% oxygen (92% nitrogen). At postnatal day 40-44, maternal SE reduced grip strength in grip traction and foot fault tests, which were also reduced by HI injury to similar levels regardless of the maternal group. Limb coordination was impaired by maternal SE which was not worsened by HI injury. Maternal SE increased anxiety level in the offspring, which was normalized by HI injury. Apoptosis markers were increased in different brain regions by maternal SE, with the cortex having further increased TUNEL by HI injury, along with increased markers of inflammation and mitophagy. We conclude that maternal SE can worsen HI-induced cellular damage in male offspring well into adolescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.