Olfactory ensheathing cell apoptosis induced by hypoxia and serum deprivation.

Yanhong Zhao, Bin Wang, Yuan Gao, Yannan Zhao, Zhifeng Xiao, Wenxue Zhao, Bing Chen, Xia Wang, Jianwu Dai
Author Information
  1. Yanhong Zhao: Key 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.

MeSH Term

Amino Acid Chloromethyl Ketones
Animals
Apoptosis
Caspase 3
Cell Count
Cells, Cultured
Dose-Response Relationship, Drug
Enzyme Inhibitors
Hypoxia
Male
Nerve Tissue Proteins
Olfactory Bulb
Rats
Rats, Sprague-Dawley
Receptors, Growth Factor
Receptors, Nerve Growth Factor
Serum
Stem Cells
Time Factors

Chemicals

Amino Acid Chloromethyl Ketones
Enzyme Inhibitors
Nerve Tissue Proteins
Receptors, Growth Factor
Receptors, Nerve Growth Factor
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
Ngfr protein, rat
Caspase 3

Word Cloud

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