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Title: LXR agonist rescued the deficit in the proliferation of the cerebellar granule cells induced by dexamethasone

Abstract

Dexamethasone (DEX) exposure during early postnatal life produces permanent neuromotor and intellectual deficits and stunts cerebellar growth. The liver X receptor (LXR) plays important roles in CNS development. However, the effects of LXR on the DEX-mediated impairment of cerebellar development remain undetermined. Thus, mice were pretreated with LXR agonist TO901317 (TO) and were later exposed to DEX to evaluate its protective effects on DEX-mediated deficit during cerebellar development. The results showed that an acute exposure of DEX on postnatal day 7 resulted in a significant impairment in cerebellar development and decreased the proliferation of granule neuron precursors in the external granule layer of cerebellum. This effect was attenuated by pretreatment with TO. We further found that the decrease in the proliferation caused by DEX occurred via up-regulation of glucocorticoid receptor and p27kip1, which could be partially prevented by LXR agonist pretreatment. Overall, our results suggest that LXR agonist pretreatment could protect against DEX-induced deficits in cerebellar development in postnatal mice and may thus be perspective recruited to counteract such GC side effects.

Authors:
; ; ; ; ; ;
Publication Date:
OSTI Identifier:
22606189
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 477; Journal Issue: 4; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ACUTE EXPOSURE; CEREBELLUM; DEXAMETHASONE; LIVER; MICE; NERVE CELLS; RECEPTORS; SIDE EFFECTS

Citation Formats

Bian, Xuting, Zhong, Hongyu, Li, Fen, Cai, Yulong, Li, Xin, Wang, Lian, and Fan, Xiaotang, E-mail: fanxiaotang2005@163.com. LXR agonist rescued the deficit in the proliferation of the cerebellar granule cells induced by dexamethasone. United States: N. p., 2016. Web. doi:10.1016/J.BBRC.2016.06.142.
Bian, Xuting, Zhong, Hongyu, Li, Fen, Cai, Yulong, Li, Xin, Wang, Lian, & Fan, Xiaotang, E-mail: fanxiaotang2005@163.com. LXR agonist rescued the deficit in the proliferation of the cerebellar granule cells induced by dexamethasone. United States. doi:10.1016/J.BBRC.2016.06.142.
Bian, Xuting, Zhong, Hongyu, Li, Fen, Cai, Yulong, Li, Xin, Wang, Lian, and Fan, Xiaotang, E-mail: fanxiaotang2005@163.com. 2016. "LXR agonist rescued the deficit in the proliferation of the cerebellar granule cells induced by dexamethasone". United States. doi:10.1016/J.BBRC.2016.06.142.
@article{osti_22606189,
title = {LXR agonist rescued the deficit in the proliferation of the cerebellar granule cells induced by dexamethasone},
author = {Bian, Xuting and Zhong, Hongyu and Li, Fen and Cai, Yulong and Li, Xin and Wang, Lian and Fan, Xiaotang, E-mail: fanxiaotang2005@163.com},
abstractNote = {Dexamethasone (DEX) exposure during early postnatal life produces permanent neuromotor and intellectual deficits and stunts cerebellar growth. The liver X receptor (LXR) plays important roles in CNS development. However, the effects of LXR on the DEX-mediated impairment of cerebellar development remain undetermined. Thus, mice were pretreated with LXR agonist TO901317 (TO) and were later exposed to DEX to evaluate its protective effects on DEX-mediated deficit during cerebellar development. The results showed that an acute exposure of DEX on postnatal day 7 resulted in a significant impairment in cerebellar development and decreased the proliferation of granule neuron precursors in the external granule layer of cerebellum. This effect was attenuated by pretreatment with TO. We further found that the decrease in the proliferation caused by DEX occurred via up-regulation of glucocorticoid receptor and p27kip1, which could be partially prevented by LXR agonist pretreatment. Overall, our results suggest that LXR agonist pretreatment could protect against DEX-induced deficits in cerebellar development in postnatal mice and may thus be perspective recruited to counteract such GC side effects.},
doi = {10.1016/J.BBRC.2016.06.142},
journal = {Biochemical and Biophysical Research Communications},
number = 4,
volume = 477,
place = {United States},
year = 2016,
month = 9
}