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Title: Nuclear orphan receptor TLX affects gene expression, proliferation and cell apoptosis in beta cells

Abstract

Nuclear orphan receptor TLX is an essential regulator of the growth of neural stem cells. However, its exact function in pancreatic islet cells is still unknown. In the present study, gene expression profiling analysis revealed that overexpression of TLX in beta cell line MIN6 causes suppression of 176 genes and upregulation of 49 genes, including a cadre of cell cycle, cell proliferation and cell death control genes, such as Btg2, Ddit3 and Gadd45a. We next examined the effects of TLX overexpression on proliferation, apoptosis and insulin secretion in MIN6 cells. Proliferation analysis using EdU assay showed that overexpression of TLX increased percentage of EdU-positive cells. Cell cycle and apoptosis analysis revealed that overexpression of TLX in MIN6 cells resulted in higher percentage of cells exiting G1 into S-phase, and a 58.8% decrease of cell apoptosis induced by 0.5 mM palmitate. Moreover, TLX overexpression did not cause impairment of insulin secretion. Together, we conclude that TLX is among factors capable of controlling beta cell proliferation and survival, which may serve as a target for the development of novel therapies for diabetes. - Highlights: • TLX overexpression in MIN6 cell causes significant expression changes of 225 genes. • TLX overexpression promotes MIN6 cellmore » proliferation and decreases cell apoptosis. • TLX overexpression does not cause impairment of insulin secretion.« less

Authors:
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Publication Date:
OSTI Identifier:
22594129
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 468; Journal Issue: 1-2; Other Information: Copyright (c) 2015 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; APOPTOSIS; CELL CYCLE; CELL PROLIFERATION; GENES; INHIBITION; INSULIN; PANCREAS; RECEPTORS; SECRETION; STEM CELLS; THERAPY

Citation Formats

Shi, Xiaoli, Xiong, Xiaokan, Dai, Zhe, Deng, Haohua, Sun, Li, Hu, Xuemei, Zhou, Feng, and Xu, Yancheng, E-mail: oxyccc@163.com. Nuclear orphan receptor TLX affects gene expression, proliferation and cell apoptosis in beta cells. United States: N. p., 2015. Web. doi:10.1016/J.BBRC.2015.10.042.
Shi, Xiaoli, Xiong, Xiaokan, Dai, Zhe, Deng, Haohua, Sun, Li, Hu, Xuemei, Zhou, Feng, & Xu, Yancheng, E-mail: oxyccc@163.com. Nuclear orphan receptor TLX affects gene expression, proliferation and cell apoptosis in beta cells. United States. doi:10.1016/J.BBRC.2015.10.042.
Shi, Xiaoli, Xiong, Xiaokan, Dai, Zhe, Deng, Haohua, Sun, Li, Hu, Xuemei, Zhou, Feng, and Xu, Yancheng, E-mail: oxyccc@163.com. Fri . "Nuclear orphan receptor TLX affects gene expression, proliferation and cell apoptosis in beta cells". United States. doi:10.1016/J.BBRC.2015.10.042.
@article{osti_22594129,
title = {Nuclear orphan receptor TLX affects gene expression, proliferation and cell apoptosis in beta cells},
author = {Shi, Xiaoli and Xiong, Xiaokan and Dai, Zhe and Deng, Haohua and Sun, Li and Hu, Xuemei and Zhou, Feng and Xu, Yancheng, E-mail: oxyccc@163.com},
abstractNote = {Nuclear orphan receptor TLX is an essential regulator of the growth of neural stem cells. However, its exact function in pancreatic islet cells is still unknown. In the present study, gene expression profiling analysis revealed that overexpression of TLX in beta cell line MIN6 causes suppression of 176 genes and upregulation of 49 genes, including a cadre of cell cycle, cell proliferation and cell death control genes, such as Btg2, Ddit3 and Gadd45a. We next examined the effects of TLX overexpression on proliferation, apoptosis and insulin secretion in MIN6 cells. Proliferation analysis using EdU assay showed that overexpression of TLX increased percentage of EdU-positive cells. Cell cycle and apoptosis analysis revealed that overexpression of TLX in MIN6 cells resulted in higher percentage of cells exiting G1 into S-phase, and a 58.8% decrease of cell apoptosis induced by 0.5 mM palmitate. Moreover, TLX overexpression did not cause impairment of insulin secretion. Together, we conclude that TLX is among factors capable of controlling beta cell proliferation and survival, which may serve as a target for the development of novel therapies for diabetes. - Highlights: • TLX overexpression in MIN6 cell causes significant expression changes of 225 genes. • TLX overexpression promotes MIN6 cell proliferation and decreases cell apoptosis. • TLX overexpression does not cause impairment of insulin secretion.},
doi = {10.1016/J.BBRC.2015.10.042},
journal = {Biochemical and Biophysical Research Communications},
number = 1-2,
volume = 468,
place = {United States},
year = {Fri Dec 04 00:00:00 EST 2015},
month = {Fri Dec 04 00:00:00 EST 2015}
}