Interleukin-3 Prevents Cellular Death Induced by Oxidative Stress in HEK293 Cells

被引:3
|
作者
Lopez, Camila [1 ]
Zamorano, Patricia [1 ]
Teuber, Stefanie [1 ]
Salas, Monica [1 ]
Otth, Carola [2 ,3 ]
Hidalgo, Maria A. [4 ]
Concha, Ilona [1 ]
Zambrano, Angara [1 ,3 ]
机构
[1] Inst Bioquim & Microbiol, Fac Ciencias, Valdivia, Chile
[2] Inst Microbiol Clin, Fac Med, Valdivia, Los Rios, Chile
[3] Univ Austral Chile, Ctr Interdisciplinary Studies Nervous Syst CISNe, Valdivia, Chile
[4] Univ Austral Chile, Fac Ciencias Vet, Inst Farmacol, Valdivia, Los Rios, Chile
关键词
IL-3; CELL SURVIVAL; PI3k/Akt; Erk; OXIDATIVE STRESS; COLONY-STIMULATING FACTOR; MALE GERM-CELLS; GM-CSF; INCREASED GLUCOSE; NEURONAL DEATH; GROWTH-FACTORS; IL-3; ACTIVATION; SURVIVAL; JAK2;
D O I
10.1002/jcb.25790
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Interleukin-3 (IL-3) is a well-characterized growth factor in hematopoietic cells, but it is also expressed in other cell types with poorly described functions. Many studies have provided evidence that IL-3 plays an important role in cell survival. We have previously shown that IL-3 is able to increase glucose uptake in HEK293 cells, suggesting that this factor requires sustained glucose metabolism to promote cell survival. In this study, we demonstrate that IL-3 contributes to cell survival under oxidative stress, a prominent feature in the pathophysiology of cancer, diabetes, and neurodegenerative diseases, as well as in the aging process. Our results suggest a molecular mechanism that involves signaling pathways mediated by PI-3k/Akt and Erk. Altogether, these findings show an important role for IL-3 in supporting the viability of non-hematopoietic systems. J. Cell. Biochem. 118: 1330-1340, 2017. (C) 2016 Wiley Periodicals, Inc.
引用
收藏
页码:1330 / 1340
页数:11
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