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.
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Shi
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China.
authors.forename: Xiaokan
authors.initials: X
authors.lastname: Xiong
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China.
authors.forename: Zhe
authors.initials: Z
authors.lastname: Dai
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China.
authors.forename: Haohua
authors.initials: H
authors.lastname: Deng
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China.
authors.forename: Li
authors.initials: L
authors.lastname: Sun
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China.
authors.forename: Xuemei
authors.initials: X
authors.lastname: Hu
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China.
authors.forename: Feng
authors.initials: F
authors.lastname: Zhou
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, PR China. Electronic address: oxyccc@163.com.
authors.forename: Yancheng
authors.initials: Y
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis; D002460:Cell Line; D049109:Cell Proliferation; D005786:Gene Expression Regulation; D007328:Insulin / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000166:cytology* / Q000378:metabolism; D051379:Mice; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D007328:Insulin; C490258:Nr2e1 protein, mouse; D018160:Receptors, Cytoplasmic and Nuclear
keywords: Apoptosis; Beta cell; Cell proliferation; Digital gene expression profile; TLX