Effect of urinary proteins and advanced glycosylation end products on ly-sosomes in renal tubular epithelial cells
10.3969/j.issn.1000-4718.2015.03.021
- VernacularTitle:尿蛋白及晚期糖基化终产物对肾小管上皮细胞溶酶体的影响
- Author:
Jiankun DENG
;
Shujun WANG
;
Hongluan WU
;
Mianna LUO
;
Bihua XU
;
Dong LIANG
;
Qingjun PAN
;
Huafeng LIU
;
Weijing LIU
- Publication Type:Journal Article
- Keywords:
Tubular epithelial cells;
Lysosome;
Urinary proteins;
Advanced glycosylation end products
- From:
Chinese Journal of Pathophysiology
2015;(3):505-510
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM:To investigate the effects of pathological products, urinary proteins and advanced glycosyla-tion end products ( AGE) produced in the progression of chronic kidney disease ( CKD) , on the structure and function of lysosomes in renal tubular epithelial cells ( TECs ) , and try to find a novel approach for preventing or delaying CKD. METHODS:The renal specimens of the untreated patients with minimal change nephrotic syndrome (MCNS), diabetic nephropathy (DN) or normal kidney were collected.The expression of lysosomal-associated membrane protein 1 (LAMP1) and cathepsin B ( CB) was studied in TECs by indirect immunofluorescent staining.Human renal tubular epithelial cell line HK-2 was incubated with 8 g/L urinary proteins or 100 mg/L AGE.The expression of LAMP1 and CB was investigated by indirect immunofluorescence and the activity of CB and cathepsin L ( CL) was measured by biochemical and enzymatic as-says.The degradation of DQ-ovalbumin was also determined.RESULTS: The lysosomal membrane permeabilization oc-curred in the TECs of MCNS and DN patients.After treatment with urinary proteins or AGE-BSA, the lysosomal membrane permeabilization of the HK-2 cells was increased.The activity of CB and CL and degradation of DQ-ovalbumin were de-creased as compared with normal control group.CONCLUSION:The digestive function of lysosome was decreased and ly-sosomal membrane permeabilization occurred in the TECs exposed to urinary proteins and AGE, which might be a key factor to induce the tubulointerstitial fibrosis.
