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Inderjeet Kaur, Sonika Rathi, Subhadra Jalali, Ramesha Kekunaya, Preeti Patil Chhablani, Divya Balakrishnan, Subhabrata Chakrabarti; Global Gene Expression Profiling in Retinopathy of Prematurity. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):957.
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© ARVO (1962-2015); The Authors (2016-present)
Retinopathy of prematurity (ROP) is a common blinding disease caused by the abnormal growth of blood vessels in the retina of premature babies with low birth weight and low gestation period. However, the mechanisms and factors contributing to the progression of ROP are still unknown. The present study aimed to identify gene(s) responsible for ROP progression by a global gene expression profiling.
From a cohort of 600 subjects comprising ROP babies (n=350) and controls (n=250), 15 ROP babies at any stage (gestational age [GA] ≤ 35 weeks and/or birth weight [BW] ≤ 1700 g) and premature babies with no ROP (n=6) (GA ≤ 35 weeks and/or BW ≤ 1700 g) and full term babies of the same age and no ROP (n=3), were screened. RNA was isolated from 0.5-1 ml of blood using RNeasy mini kit from Qiagen and the purity and integrity of RNA was checked with Bioanalyzer 2100 (Agilent). Global gene expression profiling was performed by using Illumina bead Chip array having ~47,000 transcripts. The expression profiles were studied by Gene Expression module (Gx) using the Genome Studio software and statistical analysis was done to analyze fold expression between cases and controls. Meta-analysis of differentially expressed genes were performed using Gene Ontology (GO) and Pathway analysis using the on-line PANTHER softwares, respectively.
A total of 142 genes were differentially expressed (115 genes were upregulated and 27 downregulated) between the patients with any stage of ROP compared to the no-ROP premature controls. Of these, 19 genes were expressed differentially with >2 fold and 53 genes with >1.5 fold changes, respectively. Further, the number of differentially expressed genes increased to 634 (337 upregulated and 297 downregulated) with 67 genes showing >2-fold change of expression, when non proliferative ROP subjects were included in the control group. Pathway analysis of genes (>2-fold change) showed significant differential expression, indicating the involvement of inflammation mediated by chemokine and cytokine, endothelin and toll like receptor signaling pathways, respectively.
Significant differential gene expression observed in ROP suggests the possible underlying mechanisms in the development and progression of ROP. The differentially expressed genes are currently being validated in an extended ROP cohort.
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