Activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of type II focal cortical dysplasia.
- Author:
Kun LIN
1
;
Yuan-xiang LIN
;
De-zhi KANG
;
Zhong-xing YE
;
Xing-fu WANG
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Brain Diseases; metabolism; pathology; Child, Preschool; Epilepsy; metabolism; pathology; Female; Glial Fibrillary Acidic Protein; metabolism; Humans; Immunohistochemistry; Male; Malformations of Cortical Development; metabolism; pathology; Malformations of Cortical Development, Group I; Nestin; metabolism; Neurons; metabolism; Phosphorylation; Proto-Oncogene Proteins c-akt; metabolism; Ribosomal Protein S6 Kinases, 70-kDa; metabolism; TOR Serine-Threonine Kinases; metabolism; Young Adult
- From: Chinese Journal of Pathology 2013;42(5):311-315
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether mammalian target of rapamycin (mTOR) kinase was abnormally activated in maldeveloped balloon cells and dysmorphic neurons of focal cortical dysplasia (FCD) with refractory epilepsy.
METHODSA total of 12 archival cases of FCD typeIIwith medically intractable epilepsy treated between 2008 and 2010 were retrieved. Perilesional brain tissue was used as control specimens (n = 8). The expression of phosphorylated p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was investigated by imunocytochemistry.
RESULTSThe expression of p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was found in meldeveloped balloon cells and dysmorphic neurons of FCD. A weak stain in a small amount of pyramid neurons was also found in the control group.
CONCLUSIONAbnormal activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of FCD may be a key molecular mechanism underlying the histological changes and repeated seizures.
