Related Experiment Video
Updated: Aug 14, 2025

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia
Published on: November 14, 2020
Peroxiredoxin-6 Released by Astrocytes Contributes to Neuroapoptosis During Ischemia
Jin-Yi Hou1, Xiao-Ling Zhou2, Xiao-Yuan Wang2
1Department of Neurology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China; Department of Acupuncture and Moxibustion, Xuzhou Hospital of Traditional Chinese Medicine, Xuzhou, Jiangsu 221002, China.
Abstract:
Peroxiredoxin-6 (PRDX6), a member of the peroxiredoxin family, has progressively emerged as a possible therapeutic target for a variety of brain diseases, particularly Alzheimer's disease and ischemic stroke. However, the role of PRDX6 in neurons under ischemic conditions has remained elusive. Here, we found that astrocytes could release PRDX6 extracellularly after OGD/R, and that PRDX6 release actually worsened neuroapoptosis under OGD/R. We discovered a unique PRDX6/RAGE/JNK signaling pathway that contributes to the effect of neuroapoptosis. We applied a specific inhibitor of the RAGE signaling pathway in a mouse MCAO model and observed significant alterations in animal behavior. Considered together, our findings show the crucial role of the astrocyte-released PRDX6 in the process of neuroapoptosis caused by OGD/R, and could provide novel insights for investigating the molecular mechanism of protecting brain function from ischemia-reperfusion injury.
Related Concept Videos
Necrosis
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
The Intrinsic Apoptotic Pathway
Apoptosis
Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
The Extrinsic Apoptotic Pathway
Phagocytosis of Apoptotic Cells
Normal cells contain receptors that prevent them from being recognized...

