Glucose‐induced dysregulation of lncRNAs in a model of chronic kidney disease

Abstract

Diabetic nephropathy (DN) is the leading cause for end‐stage renal disease worldwide. Despite the extensive research that has been done to identify biomarkers and novel therapeutic targets for DN, long non‐coding RNAs (lncRNAs) have not been very well studied. This study sought to identify lncRNAs that are differentially expressed in diabetic podocytes compared to normal podocytes. To do so, Human Glomerular Epithelial Cells (HGEC) were cultured in either normal or high glucose environments (5 mM and 25 mM, respectively). Differential expression of lncRNAs was detected using qPCR. HGEC cultured in high glucose levels demonstrated upregulation of MEG3, MEG8, and H19 compared to cells cultured in normal glucose. Additionally, a modest upregulation of Xist was exhibited by HGEC cultured in high glucose. No differences in MALAT1, TUG1, HOTAIR, or NEAT1 were detected. Podocalyxin, a marker of podocyte health, was used as a control. The results indicate that some lncRNAs, specifically MEG3, MEG8, Xist, and H19, are upregulated in diabetic podocytes. Further research is needed to elucidate the mechanism by which these lncRNAs contribute to the progression of DN.Support or Funding InformationThis work was supported by the Research and Development Committee of Dickinson College and by the School of Science, Engineering, and Technology of Penn State Harrisburg.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.