PIKE is essential for oligodendroglia development and CNS myelination

被引：13
|
作者：
Chan, Chi Bun [1 ]
Liu, Xia [1 ]
Zhao, Lixia [2 ]
Liu, Guanglu [2 ]
Lee, Chi Wai [3 ]
Feng, Yue [2 ]
Ye, Keiqang [1 ]
机构：
[1] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA
[2] Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA
[3] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore 117597, Singapore
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2014年 / 111卷 / 05期
基金：
美国国家卫生研究院;
关键词：
PHOSPHOINOSITIDE 3-KINASE ENHANCER; BASIC-PROTEIN; RAPAMYCIN PATHWAY; MAMMALIAN TARGET; PROGENITOR CELLS; MESSENGER-RNA; QKI; AKT; DIFFERENTIATION; REMYELINATION;
D O I：
10.1073/pnas.1318185111
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Oligodendrocyte (OL) differentiation and myelin development are complex events regulated by numerous signal transduction factors. Here, we report that phosphoinositide-3 kinase enhancer L (PIKE-L) is required for OL development and myelination. PIKE-L expression is up-regulated when oligodendrocyte progenitor cells commit to differentiation. Conversely, depleting phosphoinositide-3 kinase enhancer (PIKE) expression by shRNA prevents oligodendrocyte progenitor cell differentiation. In both conventional PIKE knockout (PIKE-/-) and OL-specific PIKE knockout mice, the number of OLs is reduced in the corpus callosum. PIKE-/- OLs also display defects when forming myelin sheath on neuronal axons during neonatal development, which is partially rescued when PTEN is ablated. In addition, Akt/mTOR signaling is impaired in OL-enriched tissues of the PIKE-/- mutant, leading to reduced expression of critical proteins for myelin development and hypomyelination. Moreover, myelin repair of lysolecithin-induced lesions is delayed in PIKE-/- brain. Thus, PIKE plays pivotal roles to advance OL development and myelinogenesis through Akt/mTOR activation.
引用
收藏
页码：1993 / 1998
页数：6
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