Abstract: PO0908
Nerve Growth Factor Protects Podocyte Apoptosis by Regulating Sirt1 Expression
Session Information
- Diabetic Kidney Disease: Basic Mechanisms
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 601 Diabetic Kidney Disease: Basic
Authors
- E, Jing, Ningxia People's Hospital, Yinchuan, Ningxia, China
- Zheng, Yali, Ningxia People's Hospital, Yinchuan, Ningxia, China
Group or Team Name
- Ningxia People' Hospital
Background
Podocyte injury contributes to the progression of diabetic kidney disease (DKD). In the previous studies, we demonstrate that expression of Cdk5/p35 play an important role in the diabetic kidney and associated with the progression of DKD in human. As know, podocyte can secret NGF and Sirt1 is one substrate of CDK5,so the objective of this article is to investigate the mechanism of NGF protecting podocyte apoptosis by regulating Sirt1 expression and to provid a new biological target for clinical treatment.
Methods
The immortalized mouse podocyte was cultured in vitro, then were transfected with control siRNA or siNGF vector to detect protein level of Sirt1 and apoptosis associated protein Cleaved caspase3 through western blot. In addition, podoctyes were also given different concentration of NGF to detect the expression of Sirt1 and Cleaved caspase 3 in order to find the relationship of NGF and Sirt1,and the role of NGF on podocytes.
Results
To understand the role of NGF on podocyte, we stimulated immortalized mouse podocytes with NGF in different concentration, the protein level of Sirt1 was positive associated with NGF expression. 2. Podocytes were transfected with control siRNA or siNGF vector by using ViaFectTM Kit, the effect of siNGF was verified by western blot. knockdown of NGF decreased the expression of Sirt1 and Cleaved caspase. 3. When gave NGF stimulation, the protein lelvel of Cleaved caspase3 was deceaed .
Conclusion
NGF plays a key role in protection podocyte by regulating the expression of Sirt1, NGF/SIRT1 axis may be a new biological target for preventing podocyte injury.
Funding
- Other NIH Support
