Abstract: PO0664
Apolipoprotein C3-Rich Low-Density Lipoprotein Is Elevated in Diabetic Kidney Disease Patients and Enhances Endothelial Cell Injury
Session Information
- Diabetic Kidney Disease: Basic - I
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 601 Diabetic Kidney Disease: Basic
Authors
- Wang, Jie Sian, Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
- Tsai, Ping Hsuan, Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
- Tseng, Kuo Feng, Department of Biological Science and Technology, China Medical University, Taichung, Taiwan
- Chen, Fang Yu, Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
- Shen, Ming-Yi, Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
Group or Team Name
- MYS Fat Research Lab
Background
Diabetic dyslipidemia plays a pathogenetic role in the development and perpetuation of diabetic kidney disease (DKD). Apolipoprotein CIII (ApoC3), a component of some triglyceride-rich very-low-density and low-density lipoprotein, expression by glucose may contribute to diabetic dyslipidemia. Early endothelial damage is also associated with progression of DKD. Thus, we want to study the effect of ApoC3-rich low-density lipoprotein (AC3RL) on DKD and its underlying molecular mechanisms.
Methods
Plasma samples were obtained from clinically stable patients with DKD recruited at our outpatient clinic. AC3RL was isolated from plasma low-density lipoprotein with the affinity-purified method.
Results
Level of plasma AC3RL were significantly higher in DKD patients than in control subjects (Figure; p<0.05). AC3RL induced endothelial cells (ECs) apoptosis and reduction of the fenestrated endothelium. The level of phosphorylation of IKKa, p53 and Cleaved Caspase-3 (CC3) were markedly increased in AC3RL-induced ECs (p < 0.05 vs. control; n = 4). The contribution of P-IKKa, p53, and CC3 in AC3RL-mediated apoptosis were blocked in ECs transfected with si-IKKa.
Conclusion
AC3RL elevation may be a risk factor for DKD, and inhibiting IKKa may be novel protect endothelial damage and arrest DKD progression.
Funding
- Clinical Revenue Support