Related Experiment Video
Updated: Jul 3, 2026
Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue
Published on: March 4, 2015
c-Abl is involved in high glucose-induced apoptosis in embryonic E12.5 cortical neural progenitor cells from the
De-Yong Jia1, Zhan-Hui Du, Shang-Ming Liu
1Key Laboratory of the Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School of Medicine, China.
Abstract:
Hyperglycemia causes direct apoptosis of neural progenitor cells (NPCs) in diabetic-induced neural tube defects in embryos. However, the underlying mechanisms are poorly understood. The present study is aimed to investigate the specific cellular proteins that may be involved in NPCs apoptosis as well as mechanisms by which the proteins regulate the oxidative stress-induced NPCs apoptosis. Our present results have shown that the expression of c-Abl was up-regulated in NPCs exposed to high glucose in vitro. The increased c-Abl was localized mainly in the nucleus. High glucose also induced an increase in nuclear p53 protein levels and the p53-c-Abl complex in NPCs. Administration of reactive oxygen species scavengers decreased the protein level of c-Abl, p53 and NPCs apoptosis. Inhibition of c-Abl reduced NPCs apoptosis and the nuclear protein level of p53 in response to high glucose. These results demonstrate that c-Abl is involved in the reactive oxygen species-activated apoptotic pathways in NPCs apoptosis. Inhibition of c-Abl may protect NPCs against insults induced by high glucose via the modulation of NPCs apoptotic machinery.
Insights
High glucose induces neural progenitor cell (NPC) apoptosis via oxidative stress and c-Abl activation. Inhibiting c-Abl protects NPCs, suggesting a therapeutic target for diabetic embryopathy.
Area of Science:
- Developmental Biology
- Cellular Biology
- Neuroscience
Background:
- Hyperglycemia in diabetes mellitus can lead to neural tube defects in embryos.
- Neural progenitor cells (NPCs) undergo apoptosis under hyperglycemic conditions, but mechanisms remain unclear.
- Oxidative stress is implicated in NPC apoptosis during diabetic embryopathy.
Purpose of the Study:
- To investigate proteins involved in NPC apoptosis induced by high glucose.
- To elucidate the mechanisms by which these proteins regulate oxidative stress-induced NPC apoptosis.
- To explore the role of c-Abl in high glucose-induced NPC apoptosis.
Main Methods:
- In vitro culture of NPCs exposed to high glucose.
- Analysis of c-Abl and p53 protein expression and localization.
- Assessment of reactive oxygen species (ROS) scavenger effects.
- Evaluation of c-Abl inhibition on NPC apoptosis and protein levels.
Main Results:
- High glucose upregulated nuclear c-Abl expression in NPCs.
- High glucose increased nuclear p53 levels and the p53-c-Abl complex.
- ROS scavengers reduced c-Abl, p53, and NPC apoptosis.
- c-Abl inhibition decreased NPC apoptosis and nuclear p53 levels under high glucose.
Conclusions:
- c-Abl is a key mediator in ROS-activated apoptotic pathways in NPCs under hyperglycemic conditions.
- Inhibition of c-Abl demonstrates a protective effect on NPCs against high glucose insults.
- Modulating the NPC apoptotic machinery via c-Abl inhibition offers a potential therapeutic strategy.
More Related Videos
08:22A Novel Strategy Combining Array-CGH, Whole-exome Sequencing and In Utero Electroporation in Rodents to Identify Causative Genes for Brain Malformations
Published on: December 1, 2017
10:36Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017