Abstract: FR-PO610
MicroRNA-148b Influences High Glucose-Induced Endoplasmic Reticulum Stress in Rat Mesangial Cells by Targeting AMPKα1
Session Information
- Diabetes Mellitus and Obesity: Basic - Experimental - II
November 03, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Diabetes
- 501 Diabetes Mellitus and Obesity: Basic - Experimental
Author
- Fan, Qiuling, Department of Nephrology, The First Hospital, China Medical University, Shenyang, China
Background
To verify the expression of microRNA-148b (miRNA-148b) induced by high glucose in rat mesangial cells, and to explore its effect on its target gene AMP-activated protein kinaseα1 (AMPKα1) and extracellular matrix excretion.
Methods
Rat mesangial cells were divided into 3 groups: normal glucose (NG, 5.5 mmol/L glucose) group, hypertonic (MA, 5.5 mmol/L glucose+ 19.5 mmol/L mannitol) group and high glucose (HG, 25.0 mmol/L glucose) group. miR-148b expression
was detected by real time PCR. Then miR-148b inhibitor was transfected to rat mesangial cells. Their expressions of AMPKα1, glucose regulated protein78 (GRP78), C/EBP homologous protein (CHOP), fibronectin (FN)and collagen 4 proteins were detected by Western blotting; the expression of AMPKα1 mRNA was detected by real time PCR; the expression of COl 4 was also detected by immunofluorescence.
Results
Compared with NG group, HG group showed upregulated miR-148b expression, downregulated AMPKα1 mRNA and protein expression, and upregulated CHOP, GRP78,collagen 44 and FN expression (all P＜0.05). HG-induced mesangial cells with miR-148b inhibitor had up-regulated AMPKα1 mRNA and protein expression, and downregulated CHOP, GRP78,collagen 4, FN expression as compared with HG-induced cells without miR-148b inhibitor (all P＜0.05).
Conclusion
HG can upregulate miR-148b expression and downregulate AMPKα1 expression in rat mesangial cells, then activate endoplasmic reticulum stress to induce extracellular matrix excretion. miR-148b inhibitor upregulates AMPKα1 expression, inhibits endoplasmic reticulum stress and reduces extracellular matrix excretion.