Hyperphosphorylation of tau protein in the ipsilateral thalamus after focal cortical infarction in rats.
Hyperphosphorylation of tau has been considered as an important risk factor for neurodegenerative diseases. It has been found also in the cortex after focal cerebral ischemia. The present study is aimed at investigating changes of tau protein expression in the ipsilateral thalamus remote from the primary ischemic lesion site after distal middle cerebral artery occlusion (MCAO). The number of neurons in the ventroposterior thalamic nucleus (VPN) was evaluated using Nissl staining and neuronal nuclei (NeuN) immunostaining. Total tau and phosphorylated tau at threonine 231 (p-T231-tau) and serine 199 (p-S199-tau) levels, respectively, in the thalamus were measured using immunostaining and immunoblotting. Moreover, apoptosis was detected with terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling (TUNEL) assay. It was found that the numbers of intact neurons and NeuN(+) cells within the ipsilateral VPN were reduced significantly compared with the sham-operated group, but the levels of p-T231-tau and p-S199-tau in the ipsilateral thalamus were increased significantly in rats subjected to ischemia for 3 days, 7 days and 28 days. Furthermore, the number of TUNEL-positive cells was increased in the ipsilateral VPN at 7 days and 28 days after MCAO. Thus, hyperphosphorylated tau protein is observed in ipsilateral thalamus after focal cerebral infarction in this study. Our findings suggest that the expression of hyperphosphorylated tau protein induced by ischemia may be associated with the secondary thalamic damage after focal cortical infarction via an apoptotic pathway.
Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, Guangdong, China; Department of Central Nervous System Regeneration, Guangdong-Hongkong-Macau Institute of CNS Regeneration (GHMICR), Jinan University, Guangzhou 510632, Guangdong, China.
Da-Wei
DW
Dong
Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, Guangdong, China.
Yu-Sheng
YS
Zhang
Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, Guangdong, China.
Wan-Yong
WY
Yang
Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, Guangdong, China.
Run-Qi
RQ
Wang-Qin
Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, Guangdong, China; Brain Science Institute, Jinan University, Guangzhou, Guangdong, China. Electronic address: andingxu63@gmail.com.
An-Ding
AD
Xu
Department of Central Nervous System Regeneration, Guangdong-Hongkong-Macau Institute of CNS Regeneration (GHMICR), Jinan University, Guangzhou 510632, Guangdong, China; Department of Human Anatomy, Jinan University School of Medicine, Guangzhou, Guangdong, China. Electronic address: tyiwen@jnu.edu.cn.
Yi-Wen
YW
Ruan
D000818:Animals; D002540:Cerebral Cortex / Q000473:pathology*; D002544:Cerebral Infarction / Q000209:etiology / Q000473:pathology*; D004195:Disease Models, Animal; D007839:Functional Laterality / Q000502:physiology*; D020287:In Situ Nick-End Labeling; D020244:Infarction, Middle Cerebral Artery / Q000150:complications; D008297:Male; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D018709:Statistics, Nonparametric; D013778:Tetrazolium Salts; D013788:Thalamus / Q000378:metabolism*; D013997:Time Factors; D016875:tau Proteins / Q000378:metabolism*
D013778:Tetrazolium Salts; D016875:tau Proteins; C009591:triphenyltetrazolium; D010751:Phosphopyruvate Hydratase
Hyperphosphorylation; Ischemia; Rat; Tau protein; Thalamus