Abstract
Retinopathy of prematurity (ROP) remains a major problem for many preterm infants. MicroRNAs (miRNAs) are a class of small noncoding RNAs that regulate gene expression at the posttranscriptional level and have been studied in many diseases. To understand the roles of miRNAs in ROP model rats, we constructed two small RNA libraries from the plasma of hyperoxia-induced rats and normal controls. Sequencing data revealed that 44 down-regulated microRNAs and 22 up-regulated microRNAs from the hyperoxia-induced rats were identified by deep sequencing technology. Some of the differentially expressed miRNAs were confirmed by quantitative reverse transcription-PCR (qRT-PCR). A total of 594 target genes of the differentially expressed microRNAs were identified using a bioinformatics approach. Functional annotation analysis indicated that a number of pathways might be involved in angiogenesis, cell proliferation and cell differentiation, which might be involved in the genesis and development of ROP. The elevated expression level of the vascular endothelial growth factor (VEGF) protein in the hyperoxia-induced neonatal rats was also confirmed by enzyme linked immunosorbent assay (ELISA). This study provides some insights into the molecular mechanisms that underlie ROP development, thereby aiding the diagnosis and treatment of this disease.
Highlights
The exposure of premature infants to hyperoxia or the relative hyperoxia of the nonuterine environment is associated with retinopathy
The second phase is induced by hypoxia, which causes elevated levels of growth factors, such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1) with resultant vaso-proliferation, neovascularization, and potential retinal detachment with subsequent vision loss [4]
The relative hyperoxia followed by repetitive hypoxic episodes that is so common in preterm infants appears to play an important role in the development of retinopathy of prematurity (ROP) [5]
Summary
The exposure of premature infants to hyperoxia or the relative hyperoxia of the nonuterine environment is associated with retinopathy. The relative hyperoxia followed by repetitive hypoxic episodes that is so common in preterm infants appears to play an important role in the development of ROP [5]. The understanding of this biphasic etiology of ROP has been enhanced by the development of rat pup models because the retinal vasculature of the newborn rat pup, which develops during the first two weeks of postnatal life, resembles that of a preterm infant [6]. In mouse models of oxygen-induced retinopathy (OIR), miRNAs regulate retinal angiogenesis via the post-transcriptional modification of genes involved in the angiogenic response to hypoxia [17,18]. We constructed two small RNA libraries from plasma samples from rat models of hypoxia and controls. This study provides an improved understanding of the mechanism of ROP
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