Knockdown of IOP1 Induces Premature Senescence in Primary HUVECs
10.13865/j.cnki.cjbmb.2021.03.1618
- Author:
Jia-Xin LIU
1
;
Fang GUO
1
;
Ling-Yue KONG
1
;
Xin-Guang LIU
1
;
Wei ZHAO
1
;
Jia-Xin LIU
2
;
Fang GUO
2
;
Ling-Yue KONG
2
;
Xin-Guang LIU
2
;
Wei ZHAO
2
Author Information
1. Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics
2. Institute of Aging Research, Guangdong Medical University
- Publication Type:Journal Article
- Keywords:
human umbilical vein endothelial cells (HUVECs);
iron-only hydrogenase-like protein 1(IOP1);
knockdown;
senescence
- From:
Chinese Journal of Biochemistry and Molecular Biology
2021;37(5):609-616
- CountryChina
- Language:Chinese
-
Abstract:
Iron-only hydrogenase-like protein 1 (IOP1) is a component of the cytosolic iron-sulfur protein assembly (CIA) machinery. IOP1 has been suggested to be a negative regulator of the hypoxia-inducible transcription factor 1(HIF-1). We previously reported that loss of one copy of NAR1 (the yeast homolog of IOP1) in diploid yeast cells leads to increased sensitivity to oxidative stress and decreased replicative lifespan‚ however‚ the underlying mechanism is still unclear. Recently‚ we found that the IOP1 protein was upregulated in late-passaged primary human umbilical vein endothelial cells (HUVECs) compared with that in early-passaged primary HUVECs‚ which indicated a potential association of IOP1 with cellular senescence. The aim of this study was to investigate the potential function of IOP1 in aging in mammalian cells. The primary HUVECs were transfected with IOP1-specific siRNA and subjected to premature senescence assays. We found that IOP1 knockdown leads to premature senescence and decreased cell proliferative ability (P < 0. 01) in primary HUVECs. Further studies revealed that downregulation of IOP1 resulted in upregulated ROS levels (P < 0. 01)‚ enhanced DNA damage (P<0. 05) and decreased mitochondrial respiration (P<0. 01) along with cell cycle arrest at the G
