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Updated: Jul 14, 2026

Transplantation of Olfactory Ensheathing Cells to Evaluate Functional Recovery after Peripheral Nerve Injury
Published on: February 23, 2014
Olfactory ensheathing cell apoptosis induced by hypoxia and serum deprivation
Yanhong Zhao1, Bin Wang, Yuan Gao
1Key laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100080, People's Republic of China.
Abstract:
Olfactory ensheathing cell (OEC) transplantation is one promising technology for the treatment of spinal cord injury. Many studies have been focusing on the functional improvement after OEC implantation in spinal cord injury of animals. However, little is known about the mechanisms about how OECs respond to the proapoptotic microenvironment after transplantation. We use the hypoxia and serum deprivation (HSD) paradigm in OECs to evaluate the effects of the ischemic damage. OECs underwent caspase-dependent apoptosis during HSD and a pan-caspase inhibitor specifically blocked the cell death. In addition, HSD resulted in a time-dependent decrease of mitochondrial membrane potential DeltaPsi(m), triggering a transient increase in p53 content and activated p53 in a time-dependent manner. In summary, our data suggest that HSD trigger apoptotic OECs death, which may be related to mitochondria dysfunction and the dependence of p53.
Insights
Olfactory ensheathing cells (OECs) undergo apoptosis when exposed to hypoxia and serum deprivation (HSD), a condition mimicking spinal cord injury. This cell death involves caspase activation, mitochondrial dysfunction, and p53 pathway activation.
Area of Science:
- Neuroscience
- Cell Biology
- Regenerative Medicine
Background:
- Olfactory ensheathing cell (OEC) transplantation shows promise for spinal cord injury (SCI) repair.
- Mechanisms of OEC survival in the hostile SCI microenvironment remain unclear.
Purpose of the Study:
- To investigate OEC response to ischemic conditions relevant to SCI.
- To elucidate the molecular pathways involved in OEC apoptosis under stress.
Main Methods:
- OECs were subjected to hypoxia and serum deprivation (HSD) to simulate ischemic damage.
- Caspase activity, mitochondrial membrane potential (ΔΨm), and p53 levels were assessed.
Main Results:
- HSD induced caspase-dependent apoptosis in OECs.
- A decrease in ΔΨm and a time-dependent increase in p53 were observed.
- Pan-caspase inhibition blocked HSD-induced cell death.
Conclusions:
- OECs undergo apoptosis under simulated ischemic conditions (HSD).
- Mitochondrial dysfunction and p53 activation are key mediators of OEC death.
- Understanding these mechanisms is crucial for optimizing OEC-based SCI therapies.
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