Higd1a Protects Cells from Lipotoxicity under High-Fat Exposure.

Abstract:

:Hypoxia-inducible gene domain family member 1A (Higd1a) has recently been reported to protect cells from hypoxia by helping to maintain normal mitochondrial function. The potential induction of Higd1a under high-fat exposure and whether it could protect cells from oxidative stress attracted our attention. Initially, 0.4 mM oleic acid and 0.2 mM palmitate were added to the growth media of HepG2 and LO2 cells for 72 hours. We discovered increased Higd1a expression, and knocking down Higd1a impaired mitochondrial transmembrane potential and induced cell apoptosis. We then identified that elevated reactive oxygen species (ROS) is responsible for increased Higd1a expression. Furthermore, we found that ROS promoted Higd1a expression by upregulating HIF-1a and PGC-1a expressions, and these two proteins could exert synergistic effects in inducing Higd1a expression. Taken together, these data suggest that Higd1a plays positive roles in protecting cells from oxidative stress, and ROS could induce Higd1a expression by upregulating PGC-1a and HIF-1a expressions.

journal_name

Oxid Med Cell Longev

authors

Li T,Xian WJ,Gao Y,Jiang S,Yu QH,Zheng QC,Zhang Y

doi

10.1155/2019/6051262

subject

Has Abstract

pub_date

2019-04-08 00:00:00

pages

6051262

eissn

1942-0900

issn

1942-0994

journal_volume

2019

pub_type

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