Melatonin promotes the acquisition of neural identity through extracellular-signal-regulated kinases 1/2 activation

被引：15

作者：

Chen, Xueran ^{[1
]}

Li, Xian ^{[1
,2
]}

Du, Zhaoxia ^{[1
]}

Shi, Wei ^{[1
]}

Yao, Yao ^{[1
]}

Wang, Chen ^{[1
]}

He, Kun ^{[1
]}

Hao, Aijun ^{[1
]}

机构：

[1] Shandong Univ, Sch Med, Dept Histol & Embryol, Key Lab,Minist Educ Expt Teratol,Shandong Prov Ke, Jinan 250012, Shandong, Peoples R China

[2] Shandong Univ, Sch Med, Dept Neurobiol, Shandong Prov Key Lab Mental Disorders, Jinan 250012, Shandong, Peoples R China

来源：

JOURNAL OF PINEAL RESEARCH | 2014年 / 57卷 / 02期

基金：

中国国家自然科学基金;

关键词：

extracellular-signal-regulated kinases 1/2; melatonin; neural determination; primitive ectoderm; Sox2; EMBRYONIC STEM-CELLS; FATE SPECIFICATION; DIFFERENTIATION; INDUCTION; SOX2; PROLIFERATION; NEUROGENESIS; PROTEIN; AGGREGATION; INHIBITION;

D O I：

10.1111/jpi.12153

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Melatonin, a major pineal secretory product, exerts a range of physiological and neuroprotective effects. However, the functional significance of melatonin in determining neural identity, and the mechanisms by which this may occur, is unknown. In this study, P19 cells were used as a model system and cell behavior was monitored. Our data show that melatonin plays an important role in determining cell fate during neural commitment and promoting the differentiation of pluripotent P19 cells (Oct4(+) Sox2(+)) into neural stem cells (Oct4(-)Sox2(+)). This promotion appears to coincide with the activation of the MT1 receptor and phosphorylation of extracellular-signal-regulated kinases 1/2 (ERK1/2). Furthermore, our results show that melatonin regulates neural fate specification of P19 cells through two distinct mechanisms: the promotion of nuclear localization of ERK1/2 and upregulation of Sox2 transcription, and suppression of Smad1-induced expression of mesodermal-specific genes, such as Bra.

引用

页码：168 / 176

页数：9

共 51 条

[31] Melatonin treatment increases the transcription of cell proliferation-related genes prior to inducing cell death in C6 glioma cells in vitro [J].