Abstract
BackgroundMaternal smoking is a risk factor for low birth weight and other adverse developmental outcomes.ObjectiveWe sought to determine the impact of standard tobacco cigarettes and e-cigarettes on heart development in vitro and in vivo.MethodsZebrafish (Danio rerio) were used to assess developmental effects in vivo and cardiac differentiation of human embryonic stem cells (hESCs) was used as a model for in vitro cardiac development.ResultsIn zebrafish, exposure to both types of cigarettes results in broad, dose-dependent developmental defects coupled with severe heart malformation, pericardial edema and reduced heart function. Tobacco cigarettes are more toxic than e-cigarettes at comparable nicotine concentrations. During cardiac differentiation of hESCs, tobacco smoke exposure results in a delayed transition through mesoderm. Both types of cigarettes decrease expression of cardiac transcription factors in cardiac progenitor cells, suggesting a persistent delay in differentiation. In definitive human cardiomyocytes, both e-cigarette- and tobacco cigarette-treated samples showed reduced expression of sarcomeric genes such as MLC2v and MYL6. Furthermore, tobacco cigarette-treated samples had delayed onset of beating and showed low levels and aberrant localization of N-cadherin, reduced myofilament content with significantly reduced sarcomere length, and increased expression of the immature cardiac marker smooth muscle alpha-actin.ConclusionThese data indicate a negative effect of both tobacco cigarettes and e-cigarettes on heart development in vitro and in vivo. Tobacco cigarettes are more toxic than E-cigarettes and exhibit a broader spectrum of cardiac developmental defects.
Highlights
Maternal smoking is one of the most significant causes of preventable perinatal morbidity and mortality worldwide, accounting for nearly $200 billion in health care costs each year within the United States alone[1]
Zebrafish (Danio rerio) were used to assess developmental effects in vivo and cardiac differentiation of human embryonic stem cells was used as a model for in vitro cardiac development. Exposure to both types of cigarettes results in broad, dose-dependent developmental defects coupled with severe heart malformation, pericardial edema and reduced heart function
Tobacco cigarettes are more toxic than E-cigarettes and exhibit a broader spectrum of cardiac developmental defects
Summary
Maternal smoking is one of the most significant causes of preventable perinatal morbidity and mortality worldwide, accounting for nearly $200 billion in health care costs each year within the United States alone[1]. Studies have shown that maternal smoking is strongly associated with placental developmental deficits, ectopic implantation, stillbirth, reduced birth weight, structural malformations as well as systemic disorders including postnatal neurobehavioral and cardiovascular problems and increased risk of Sudden Infant Death Syndrome (SIDS) [2,3,4]. Tobacco cigarette smoke has over 7,000 chemicals, including at least 69 known carcinogens such as tar, heavy metals, polycyclic aromatic hydrocarbons, phenol, benzene, carbon monoxide, nitrosamines, and hydrogen cyanide distributed throughout the gas and particulate phases [4]. The complexity of these chemical components and their interactions with each other in the context of human physiology are not well understood. Maternal smoking is a risk factor for low birth weight and other adverse developmental outcomes.
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