Abstract: SA-PO448
Dysregulated miR-936 as a Novel Diagnostic Marker for Diabetic Nephropathy: Meta-Analysis and Validation Study
Session Information
- Diabetic Kidney Disease: Basic - II
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 701 Diabetic Kidney Disease: Basic
Authors
- Garmaa, Gantsetseg, Semmelweis Egyetem, Budapest, Hungary
- Budnuc, Stefania, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania
- Kói, Tamás, Department of Stochastics, Institute of Mathematics, Budapest University of Technology and Economics, Budapest, Hungary
- Kokeny, Gabor, Semmelweis Egyetem, Budapest, Hungary
Background
MiRNAs are short non-coding ribonucleic acid molecules that bind to target messenger RNAs, resulting in their degradation and translational repression. They could be used as a diagnostic marker and nucleic acid therapy in chronic kidney disease (CKD).
Methods
We used two consecutive methods to validate miR-936 in diabetic nephropathy (DN). First, investigating potential miRNA in CKD is explored from a meta-analysis of 32 miRNA profiling studies. The enrichment analysis was performed for target genes and molecular pathways utilizing DIANA mirPath v.3 and Reactome. Finally, for the first time, miR-936 was validated by qRT-PCR in kidney biopsy of DN patients and high glucose-induced HK-2 cells.
Results
Urinary miR-936 was one of the most down-regulated from a meta-analysis (Figure 1). The enrichment analysis found dysregulated miRNAs affecting fatty acid biosynthesis and metabolism pathways. MiR-936 was over-expressed in DN patient kidney biopsies (DN, n=3) compared to control kidney tissue (CTL, n=3) but did not reach statistical significance (Mann-Whitney test). HK-2 cells in high glucose (24 hours, 25 mmol/l, n=3) medium increased miR-936 expression by 2-fold (*p<0.05 by Kruskal Wallis test), while mannitol, osmotic control (20 mmol/l, n=3) had no effect.
Conclusion
The dysregulation of miR-936 expression in diabetic nephropathy is investigated, which will provide further research on the molecular mechanism of dysregulated miR-936 in diabetic nephropathy.
Funding
- Government Support – Non-U.S.