ArticleScientific reports2015
High glucose environment inhibits cranial neural crest survival by activating excessive autophagy in the chick embryo.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Maternal obesity and metabolic disorders associate with congenital heart defects in the offspring: A systematic review.PloS one · 2021Pooled it
- Craniofacial development: genetics, signaling pathways, teratogenic mechanisms, and clinal significance.Molecular biomedicine · 2026Review
- Acute exposure to electronic cigarette components alters mRNA expression of pre-osteoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Maternal obesity: sex-specific in utero changes in fetal brain autophagy and mTOR.Obesity (Silver Spring, Md.) · 2024Article
- Cell Death, by Any Other Name….Cells · 2024Review
- Exploring the origins of neurodevelopmental proteasomopathies associated with cardiac malformations: are neural crest cells central to certain pathological mechanisms?Frontiers in cell and developmental biology · 2024Article
- Baicalin administration could rescue high glucose-induced craniofacial skeleton malformation by regulating neural crest development.Frontiers in pharmacology · 2024Article
- Cholesterol biosynthesis modulates differentiation in murine cranial neural crest cells.Scientific reports · 2023Article
- The combination of high glucose and LPS induces autophagy in bovine kidney epithelial cells via the Notch3/mTOR signaling pathway.BMC veterinary research · 2022Article
- Zebrafish models of alx-linked frontonasal dysplasia reveal a role for Alx1 and Alx3 in the anterior segment and vasculature of the developing eye.Biology open · 2022Article
- Riboceine Rescues Auranofin-Induced Craniofacial Defects in Zebrafish.Antioxidants (Basel, Switzerland) · 2021Article
- Neural crest metabolism: At the crossroads of development and disease.Developmental biology · 2021Review
- Augmented BMP signaling commits cranial neural crest cells to a chondrogenic fate by suppressing autophagic β-catenin degradation.Science signaling · 2021Article
- Role of Maternal Infections and Inflammatory Responses on Craniofacial Development.Frontiers in oral health · 2021Review
- Diabetes, Oxidative Stress, and DNA Damage Modulate Cranial Neural Crest Cell Development and the Phenotype Variability of Craniofacial Disorders.Frontiers in cell and developmental biology · 2021Review
- Maternal Obesity and Diabetes Mellitus as Risk Factors for Congenital Heart Disease in the Offspring.Journal of the American Heart Association · 2020Review
- Baicalin rescues hyperglycemia-induced neural tube defects via targeting on retinoic acid signaling.American journal of translational research · 2020Article
- LKB1 specifies neural crest cell fates through pyruvate-alanine cycling.Science advances · 2019Article
- Molecular dissection of CHARGE syndrome highlights the vulnerability of neural crest cells to problems with alternative splicing and other transcription-related processes.Transcription · 2019Review
- RIPK2-Mediated Autophagy and Negatively Regulated ROS-NLRP3 Inflammasome Signaling in GMCs Stimulated with High Glucose.Mediators of inflammation · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High glucose levels induced by maternal diabetes could lead to defects in neural crest development during embryogenesis, but the cellular mechanism is still not understood. In this study, we observed a defect in chick cranial skeleton, especially parietal bone development in the presence of high glucose levels, which is derived from cranial neural crest cells (CNCC). In early chick embryo, we found that inducing high glucose levels could inhibit the development of CNCC, however, cell proliferation was not significantly involved. Nevertheless, apoptotic CNCC increased in the presence of high levels of glucose. In addition, the expression of apoptosis and autophagy relevant genes were elevated by high glucose treatment. Next, the application of beads soaked in either an autophagy stimulator (Tunicamycin) or inhibitor (Hydroxychloroquine) functionally proved that autophagy was involved in regulating the production of CNCC in the presence of high glucose levels. Our observations suggest that the ERK pathway, rather than the mTOR pathway, most likely participates in mediating the autophagy induced by high glucose. Taken together, our observations indicated that exposure to high levels of glucose could inhibit the survival of CNCC by affecting cell apoptosis, which might result from the dysregulation of the autophagic process.
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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.