标题：High glucose induces apoptosis in embryonic neural progenitor cells by a pathway involving protein PKCδ
作者：Liu, S.;Yuan, Q.;Zhao, S.;Wang, J.;Guo, Y.;Wang, F.;Zhang, Y.;Liu, Q.;Zhang, S.;Ling, E.-A.;Hao, A.
作者机构：Department of Histology and Embryology, Key Laboratory of the Ministry of Education for Experimental Teratology, Shandong Univer
通讯作者地址：[Hao, AJ]Shandong Univ, Sch Med, Dept Histol & Embryol, Key Lab Minist Educ Expt Teratol, 44 Wenhua Xi Rd, Jinan 250012, Shandong, Peoples R China.
关键词：Apoptosis;C-Abl;High glucose;Neural progenitor cells;P53;PKCδ
摘要：Diabetic-induced neural tube defects in embryos are caused by apoptosis of neural progenitor cells (NPCs); however, the underlying mechanisms are poorly understood. The present study is aimed to investigate the specific cellular proteins that may be involved in apoptosis of NPCs. We show here that hyperglycemia-induced apoptosis of NPCs was through a PKCδ-dependent mechanism. Tyrosine phosphorylation of PKCδ was required for PKCδ binding to c-Abl in the cytoplasm, and inhibition of c-Abl by STI571 or knock-down of c-Abl by RNAi decreased the phosphorylation of PKCδ. Moreover, translocation of PKCδ and c-Abl complex from the cytoplasm to the nucleus, was blocked by down-regulation of PKCδ or c-Abl. Furthermore, we found that interaction of PKCδ and c-Abl played a crucial role in p53 accumulation in the nucleus, which was linked to the apoptosis of NPCs in response to high glucose.