Nicotine exposure during differentiation causes inhibition of N-myc expression

@article{BenYehudah2013NicotineED,
  title={Nicotine exposure during differentiation causes inhibition of N-myc expression},
  author={Ahmi Ben-Yehudah and Becki Michelle Campanaro and Laura M Wakefield and Tia N Kinney and Jill Brekosky and Vonya M. Eisinger and Carlos A. Castro and Diane L. Carlisle},
  journal={Respiratory Research},
  year={2013},
  volume={14},
  pages={119 - 119},
  url={https://api.semanticscholar.org/CorpusID:13593342}
}
This study is the first to use primate ESC to demonstrate that nicotine can affect cellular differentiation from pluripotency into fibroblasts, and in particular, mediate N-myc expression in differentiating ESCs.

Electronic Cigarette Smoke Impairs Normal Mesenchymal Stem Cell Differentiation

Both smoke extracts prevented osteogenic differentiation from progressing, evident by decreased expression of terminal osteogenic markers and mineralization, and e-cigarettes present similar risk as combustible cigarettes with respect to tissue repair impairment.

Enhanced vulnerability of the developing lungs by moderate prenatal cigarette smoke upon postnatal injury

It is observed that moderate prenatal cigarette smoke, enhances the vulnerability of the developing lung to postnatal injury resulting in impaired septation and vessel growth along with disturbed platelet drive growth factor (PDGF) signaling and extracellular matrix (ECM) remodeling.

Impact of Tobacco Smoke and Nicotine Exposure on Lung Development.

This review examines the role of prenatal and postnatal tobacco smoke and nicotine exposure and its association with augmenting infection risk, skewing the immune response toward a T-helper type 2 bias and increasing risk for developing an allergic phenotype and asthmalike symptoms during childhood.

Expression and function of nicotinic acetylcholine receptors in stem cells

This review summarizes the expression and function of known nicotinic acetylcholine receptors in different classes of stem cells including: pluripotent stem cells, mesenchymalstem cells, periodontal ligament derived stem cells and neural progenitor cells and discusses the potential downstream effects of receptor activation on stem cell function.

Tobacco Smoking During Pregnancy Is Associated With Increased Risk of Moderate/Severe Bronchopulmonary Dysplasia: A Systematic Review and Meta-Analysis

It is suggested that tobacco smoking during pregnancy increases the risk of moderate/severe BPD, and the hypothesis of the involvement of prenatal insults in the etiopathogenesis of BPD is reinforced.

Nicotinic Acetylcholine Receptor-Mediated Signaling Pathways in Pluripotent Stem Cells

Nicotinic Acetylcholine Receptor-Mediated Signaling Pathways in Pluripotent Stem Cells Takashi Yazawa , department of Biochemistry, Asahikawa Medical University, Japan.

Nmyc plays an essential role during lung development as a dosage-sensitive regulator of progenitor cell proliferation and differentiation

It is shown that Nmyc expression in the embryonic lung is normally restricted to a distal population of undifferentiated epithelial cells, a high proportion of which are in the S phase of the cell cycle, which is relevant to clinical disorders such as bronchopulmonary dysplasia of premature babies and lung cancer.

Effect of nicotine on the proliferation and differentiation of mouse induced pluripotent stem cells.

The molecular mechanisms that regulate the proliferation and differentiation of induced pluripotent stem (iPS) cells are of great interest. However, whether stimulation with nicotine enhances the

Long-term Exposure to Nicotine, via Ras Pathway, Induces Cyclin D1 to Stimulate G1 Cell Cycle Transition*

It is indicated that by targeting the Ras pathway, long-term exposure to nicotine disrupts cell cycle restriction machinery and thus potentiates tumor development.

Human embryonic stem cell-derived test systems for developmental neurotoxicity: a transcriptomics approach

The ESNATS assay battery allows classification of human DNT/RT toxicants on the basis of their transcriptome profiles and a relatively large ‘common response’ to VPA and MeHg could be distinguished from ‘compound-specific’ responses.

Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells.

Redundant Akt activation by nicotine and NNK could contribute to tobacco-related carcinogenesis by regulating two processes critical for tumorigenesis, cell growth and apoptosis.

A targeted mutation reveals a role for N-myc in branching morphogenesis in the embryonic mouse lung.

Analysis of N-myc expression in wild-type and homozygous mutant embryonic lungs suggests that N- myc is required for the proliferation of the lung epithelium in response to local inductive signals emanating from the lung mesenchyme.
...