Advanced glycation end‑products reduce podocyte adhesion by activating the renin‑angiotensin system and increasing integrin‑linked kinase

Cheng,Cailian; Zheng,Zhenda; Shi,Chenggang; Liu,Xun; Ye,Zengchun; Lou,Tanqi

doi:10.3892/etm.2013.1312

Advanced glycation end‑products reduce podocyte adhesion by activating the renin‑angiotensin system and increasing integrin‑linked kinase

Authors:
- Cailian Cheng
- Zhenda Zheng
- Chenggang Shi
- Xun Liu
- Zengchun Ye
- Tanqi Lou
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Affiliations: Department of Nephrology, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510630, P.R. China, Department of Cardiology, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510630, P.R. China
Published online on: September 23, 2013 https://doi.org/10.3892/etm.2013.1312
Pages: 1494-1498

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Abstract

The aim of this study was to investigate the effects of advanced glycation end‑products (AGEs) on podocyte adhesion and the underlying mechanisms. Immortalized mouse podocytes were exposed to various conditions and podocyte adhesion was evaluated using a hexosaminidase assay. The expression levels of integrin‑linked kinase (ILK) were measured by quantitative polymerase chain reaction (qPCR) and western blotting. Treatment with AGEs resulted in a significant, concentration‑dependent reduction in podocyte adhesion (P<0.05) and an incremental rise in ILK expression up to a maximum of 100%. Pretreatment with losartan significantly prevented the upregulation of ILK and attenuated the loss of podocyte adhesion observed in podocytes exposed to AGEs (P<0.05). However, the adhesion of losartan‑treated podocytes remained lower than that of the podocytes exposed to bovine serum albumin. The results indicate that AGEs reduce podocyte adhesion via the upregulation of ILK expression, which occurs partly through activation of the renin‑angiotensin system in podocytes.

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