Protective effects of erythropoietin on tau phosphorylation induced by beta-amyloid.
Neuropathological studies have demonstrated that the presence of neurofibrillary tangles (NFTs) is one of the most prominent pathologic characteristics of Alzheimer's disease (AD). The microtubule-associated protein tau is the major component of NFTs, and its abnormal hyperphosphorylation leads to the destabilization of microtubules, impaired axonal transport, and eventual death of the neurons. The hematopoietic cytokine erythropoietin (Epo) is now considered as a viable agent with regard to central nervous system injury in a variety of cellular systems. Here we report that Epo prevented tau hyperphosphorylation in SH-SY5Y cells exposed to the beta-amyloid peptide and that this effect may depend on the PI3K/Akt-GSK-3beta pathway. This study provides new molecular insight into the neuroprotective effect of Epo and suggests its possible therapeutic role in the management of AD.
Sun
Zhi-Kun
ZK
Department of Neurology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Yang
Hong-Qi
HQ
Pan
Jing
J
Zhen
Hong
H
Wang
Zhi-Quan
ZQ
Chen
Sheng-Di
SD
Ding
Jian-Qing
JQ
D016229:Amyloid beta-Peptides / Q000378:metabolism*; D015153:Blotting, Western; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D004921:Erythropoietin / Q000494:pharmacology*; D006801:Humans; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010766:Phosphorylation; D015398:Signal Transduction; D016875:tau Proteins / Q000187:drug effects* / Q000378:metabolism
D016229:Amyloid beta-Peptides; D018696:Neuroprotective Agents; D016875:tau Proteins; D004921:Erythropoietin