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SELENOP rs3877899 Variant Affects the Risk of Developing Advanced Stages of Retinopathy of Prematurity (ROP)
Ewa Strauss1, Danuta Januszkiewicz-Lewandowska2,3, Alicja Sobaniec4
1Institute of Human Genetics, Polish Academy of Sciences, Strzeszynska 32, 60-479 Poznan, Poland.
Insights
A specific gene variant (SELENOP rs3877899A) may increase the risk of retinopathy of prematurity (ROP) and visual impairment in extremely preterm infants, potentially due to reduced selenium bioavailability.
Area of Science:
- Genetics
- Neonatology
- Ophthalmology
Background:
- Premature newborns, especially those with extremely low gestational age (ELGA) and extremely low birth weight (ELBW), face risks for oxidative-damage-related diseases.
- Conditions like retinopathy of prematurity (ROP), bronchopulmonary dysplasia (BPD), and necrotizing enterocolitis (NEC) are significant concerns for these vulnerable infants.
- The role of selenoproteins in the development of prematurity and associated diseases is not well understood.
Purpose of the Study:
- To investigate the hypothesis that variations in selenoprotein-encoding genes (SELENOP, SELENOS, GPX4) influence the risk of ROP and other comorbidities in premature infants.
- To identify genetic factors contributing to the development and progression of ROP in extremely preterm neonates.
Main Methods:
- The study included infants born at or before 32 weeks of gestational age (GA).
- Infants were grouped based on ROP onset and progression: no ROP, spontaneously remitting ROP, and ROP requiring treatment.
- Single nucleotide polymorphisms (SNPs) in relevant genes were analyzed using TaqMan SNP genotyping assays.
Main Results:
- The SELENOP rs3877899A allele was associated with ELGA (defined as <28 GA), ROP requiring treatment, and ROP unresponsive to treatment.
- Independent predictors of ROP onset and progression included RBC transfusions, ELGA, surfactant treatment, and the rs3877899A allele in conjunction with ELGA, collectively explaining 43.1% of risk variation.
- The SELENOP rs3877899A allele was linked to reduced selenium bioavailability.
Conclusions:
- The SELENOP rs3877899A allele may contribute to the risk of ROP and subsequent visual impairment in extremely preterm infants.
- Genetic variations in selenoprotein genes represent a potential factor in the pathophysiology of ROP in vulnerable neonates.
- Further research into selenium's role is warranted for understanding and managing ROP in preterm populations.
Abstract:
The significance of selenoproteins for the incidence of prematurity and oxidative-damage-related diseases in premature newborns is poorly understood. The latter are at risk for ROP as well as BPD, IVH, PDA, RDS, and NEC, which is particularly high for newborns with extremely low gestational age (ELGA) and extremely low birth weight (ELBW). This study evaluates the hypothesis that variation in the selenoprotein-encoding genes SELENOP, SELENOS, and GPX4 affects the risk of ROP and other comorbidities. The study included infants born ≤ 32 GA, matched for onset and progression of ROP into three groups: no ROP, spontaneously remitting ROP, and ROP requiring treatment. SNPs were determined with predesigned TaqMan SNP genotyping assays. We found the association of the SELENOP rs3877899A allele with ELGA (defined as <28 GA), ROP requiring treatment, and ROP not responsive to treatment. The number of RBC transfusions, ELGA, surfactant treatment, and coexistence of the rs3877899A allele with ELGA were independent predictors of ROP onset and progression, accounting for 43.1% of the risk variation. In conclusion, the SELENOP rs3877899A allele associated with reduced selenium bioavailability may contribute to the risk of ROP and visual impairment in extremely preterm infants.
