Advanced glycosylation end products promote migration of podocytes through mTORC1/uPAR pathway
10.3969/j.issn.1000-4718.2014.12.020
- VernacularTitle:晚期糖基化终产物通过mTORC1／uPAR途径促进足细胞移动
- Author:
Xiaofan TAN
;
Yuanhan CHEN
;
Chunping YU
;
Yuxiong LAI
;
Li ZHANG
;
Xingchen ZHAO
;
Hong ZHANG
;
Ting LIN
;
Ruizhao LI
;
Wei SHI
- Publication Type:Journal Article
- Keywords:
Podocytes;
Cell mobility;
Advanced glycosylation end products;
Mammalian target of rapamycin complex 1;
Receptors,urokinase-type plasminogen activator
- From:
Chinese Journal of Pathophysiology
2014;(12):2232-2237
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM: To investigate the influence of advanced glycosylation end products-modified bovine serum albumin (AGE-BSA) on mammalian target of rapamycin complex 1 (mTORC1), urokinase-type plasminogen activator re-ceptor ( uPAR) , and cell mobility in the podocytes, and to further explore the probable relationship.METHODS: The conditionally immortalized mouse podocyte cell line was cultured in vitro.MTT assay and immunofluorescence were used to analyze the cell viability and cytoskeleton of the podocytes treated with the stimuli and intervention agents.The activity of mTORC1 and the expression level of uPAR in normal podocytes and podocytes treated with control BSA or AGE-BSA were detected by Western blotting.The migration ability of the podocytes was determined by would-healing assay.Rapamycin was added to inhibit the activity of mTORC1 along with the addition of AGE-BSA to observe the changes of uPAR and the motility of podocytes.RESULTS:No significant difference of the cell viability or cytoskeleton in the podocytes treated with the stimuli and intervention agents was observed.AGE-BSA up-regulated the activity of mTORC1 and the expression of uPAR, and induced the high mobility of the podocytes.Rapamycin obviously reduced the high expression level of uPAR and the increase in the migration ability of podocytes caused by AGE-BSA treatment.CONCLUSION: AGE-BSA might cause the high migration of podocytes through the mTORC1/uPAR signaling pathway.
