ArticleNeuromolecular medicine2013
3-methylcholanthrene induces neurotoxicity in developing neurons derived from human CD34+Thy1+ stem cells by activation of aryl hydrocarbon receptor.
Article in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Potential Toxicity Risk Assessment and Priority Control Strategy for PAHs Metabolism and Transformation Behaviors in the Environment.International journal of environmental research and public health · 2022Article
- Endocrine disruptors also function as nervous disruptors and can be renamed endocrine and nervous disruptors (ENDs).Toxicology reports · 2021Review
- Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells.Neurotoxicity research · 2017Article
- Article
- Stem Cells in Neurotoxicology/Developmental Neurotoxicology: Current Scenario and Future Prospects.Molecular neurobiology · 2016Review
- An Overview on Human Umbilical Cord Blood Stem Cell-Based Alternative In Vitro Models for Developmental Neurotoxicity Assessment.Molecular neurobiology · 2016Review
- Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease.Endocrine-related cancer · 2014Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Developing neurons, derived from the human umbilical cord blood stem cells (hUCBSCs), were investigated for their stage-specific responses against 3-methylcholanthrene (MC), a well-known polycyclic aromatic hydrocarbon. Three-dimensional (3D) molecular docking demonstrates the strong hydrogen bonding and hydrophobic interactions of MC with amino acids of aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) within 4 Å and subsequent inhibition of cAMP response element-binding protein (CREB), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors. Protein-protein docking also confirms that induced levels of AHR inhibit the neurogenesis-related transcription factor (CREB) with maximum docking scores. In concurrence with in silico data, MC exposure significantly up regulates the expression and activity of AHR, CYP1A1 and glutathione S-transferase P1-1 (GSTP1-1) and down regulates the expression of CREB, AMPA and NMDA receptors in hUCBSC-derived neuronal cells at various maturity (0, 2, 4, 8 days of differentiation). MC-mediated significant down regulation in the expression of stage-specific neuronal markers (Nestin, neural cell adhesion molecule-NCAM, synaptophysin-SYP, CREB, AMPA and N-methyl-D-aspartate receptor subunit 2A-NR2A) was also noticed in cells all through the differentiation. Data identify the possible interference of MC in neuronal transmission and neurogenesis.
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Registered trials
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 OpenQuestion graph.