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Published on: April 2, 2021
Identification of Iron Homeostasis Genes Dysregulation Potentially Involved in Retinopathy of Prematurity
Xian-Qiong Luo1, Chun-Yi Zhang2, Jia-Wen Zhang1
1Department of Neonatology, Guangdong Women and Children's Hospital, Guangzhou 511400, China.
Insights
Retinopathy of prematurity (ROP) involves molecular changes in retinal cells. Hypoxia disrupts iron homeostasis, suggesting an "oxygen plus iron" mechanism contributing to this serious preterm infant disease.
Area of Science:
- Ophthalmology
- Neonatology
- Molecular Biology
Background:
- Retinopathy of prematurity (ROP) is a significant cause of vision impairment in premature infants.
- The precise molecular mechanisms driving ROP pathogenesis remain incompletely understood.
- Limited systematic studies exist on the molecular underpinnings of ROP.
Purpose of the Study:
- To investigate global gene expression changes in human fetal retinal microvascular endothelial cells (RMECs) under hypoxic conditions.
- To identify differentially expressed genes (DEGs) associated with hypoxia in RMECs.
- To elucidate potential molecular pathways involved in ROP development.
Main Methods:
- Primary RMECs were isolated from human fetal eyeballs.
- Hypoxia was induced in vitro using Cobalt Chloride (CoCl2).
- Dual-color microarray analysis identified DEGs, validated by qRT-PCR and functional enrichment analysis using Gene Ontology.
Main Results:
- 326 differentially expressed genes (DEGs) were identified between hypoxic and normoxic RMECs.
- 198 genes were upregulated, and 128 genes were downregulated under hypoxic conditions.
- Genes involved in iron ion homeostasis were significantly enriched, indicating their crucial role.
Conclusions:
- Dysregulation of iron homeostasis pathways and associated oxidative damage are implicated in ROP mechanisms.
- The findings support an "oxygen plus iron" hypothesis for ROP pathogenesis.
- This study provides novel molecular insights into ROP development, potentially guiding future therapeutic strategies.
Abstract:
Retinopathy of prematurity (ROP) is a serious disease of preterm neonates and there are limited systematic studies of the molecular mechanisms underlying ROP. Therefore, here we performed global gene expression profiling in human fetal retinal microvascular endothelial cells (RMECs) under hypoxic conditions in vitro. Aborted fetuses were enrolled and primary RMECs were isolated from eyeballs. Cultivated cells were treated with CoCl2 to induce hypoxia. The dual-color microarray approach was adopted to compare gene expression profiling between treated RMECs and the paired untreated control. The one-class algorithm in significance analysis of microarray (SAM) software was used to screen the differentially expressed genes (DEGs) and quantitative RT-PCR (qRT-PCR) was conducted to validate the results. Gene Ontology was employed for functional enrichment analysis. There were 326 DEGs between the hypoxia-induced group and untreated group. Of these genes, 198 were upregulated in hypoxic RMECs, while the other 128 hits were downregulated. In particular, genes in the iron ion homeostasis pathway were highly enriched under hypoxic conditions. Our study indicates that dysregulation of genes involved in iron homeostasis mediating oxidative damage may be responsible for the mechanisms underlying ROP. The "oxygen plus iron" hypothesis may improve our understanding of ROP pathogenesis.
