Role of Mutyh in Oxidative Stress Damage in Retinopathy of Prematurity.
10.3881/j.issn.1000-503X.16032
- Author:
Hui-Juan LI
1
;
Jie TANG
2
;
Rui CHENG
1
Author Information
1. Department of Neonatology,Children's Hospital of Nanjing Medical University,Nanjing 210000,China.
2. Department of Neonatal Surgery,Children's Hospital of Nanjing Medical University,Nanjing 210000,China.
- Publication Type:Journal Article
- Keywords:
Mutyh;
oxidative stress;
oxygen-induced retinopathy;
photoreceptor;
retinopathy of prematurity
- MeSH:
Oxidative Stress;
Animals;
Mice;
DNA Glycosylases/metabolism*;
Retinopathy of Prematurity/etiology*;
Mice, Knockout;
Disease Models, Animal;
Humans;
Mitochondria/metabolism*
- From:
Acta Academiae Medicinae Sinicae
2024;46(6):862-871
- CountryChina
- Language:English
-
Abstract:
Objective To explore the role of the base mismatch repair gene Mutyh in retinopathy of prematurity(ROP). Methods Mutyh(-/-)and wild-type(WT)mice were used for the modeling of oxygen-induced retinopathy.The retinal oxidative stress was examined,and the ultrastructures of photoreceptors and mitochondria were observed.The biomarkers of photoreceptors and mitochondria were tested.Furthermore,the photoreceptor cell line 661W was treated with hydrogen peroxide for the modeling of oxidative stress.In the cell model,and the oxidative stress and photoreceptor functions in the cells were measured. Results In both the mouse and cell models,the expression of Mutyh was up-regulated.Mutyh knockout in mice and knockdown in cells exerted negative effects on photoreceptors and mitochondria.Mutyh overexpression showed protective functions in the cell model,indicating that Mutyh played a role in repairing photoreceptors and mitochondria. Conclusions Mutyh showed the potential to become a biomarker of ROP.Increasing Mutyh expression might have therapeutic effects on ROP,which needs further validation.
