Abstract
Purpose :
Proliferative diabetic retinopathy (DR) is a sight-threatening complication of diabetes worldwide. The molecular mechanism underlying the pathogenesis of DR is not fully understood. In this study, we presented a comparative microarray analysis of whole blood RNA from patients who have over 20 years type 2 diabetes (T2D) PDR and those without any signs of DR.
Methods :
Eleven of T2D patients with over 20 years diabetes duration were enrolled into the study. The presence or absence of DR was confirmed by fundus photography and fluorescein angiography. Of the 12 of T2D patients, 6 had active proliferative DR (PDR) and 6 were absence of any signs of DR (non-DR). Total RNA was extracted from whole blood and processed for Affymetrix microarray analysis. Gene Ontology (GO) annotation was performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID) Bioinformatics Resources v6.8 (http://david.abcc.ncifcrf.gov).
Results :
A total of 54613 genes were detected in both groups, among which 1210 genes were significantly altered in PDR compared with non-DR (≥2 folds, P<0.05). GO annotation showed that the altered genes are involved in signaling pathways regulating pluripotency of stem cells, neuroactive ligand-receptor interaction, and cytokine-cytokine receptor interaction. Besides, 389 long intergenic non-coding RNAs (LincRNAs) were identified, and 28 of them were significantly altered in PDR samples. Of the 28 LincRNAs, 16 were upregulated and 12, including LINC00624, LINC00606, and LINC00692 were downregulated in PDR patients.
Conclusions :
LincRNAs are previously thought to be "dark matter" of the genome. Emerging evidence suggests that aberrant expressions of LincRNAs are associated with the development of diabetic associate cardiovascular dysfunctions. Our results suggest that LincRNAs may be critically involved in the development of PDR.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.