The effect of advanced glycosylation end products on the expression of fibronectin and the regulation of protein kinase C in human peritoneal mesothelial cells.
- Author:
Fu-Yuan HONG
1
;
Fang SUN
;
Jun LIU
;
Jian YAO
;
Yi-Xin HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Epithelium; secretion; Fibronectins; metabolism; Glycation End Products, Advanced; pharmacology; Humans; Peritoneum; cytology; Protein Kinase C; metabolism
- From: Chinese Journal of Applied Physiology 2012;28(4):365-372
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of advanced glycosylation end products (AGEs) on the production of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) in vitro and the role of protein kinase C (PKC) in this course.
METHODSThe AGE-human serum albumin (HSA) (0, 100, 500, 1 000 microg/ml) was used in culture medium to stimulate the HPMC. The mRNA level of FN was measured with real-time PCR, moreover, the protein level of FN in HPMC was detected by ELISA. With the method of ELISA, the PKC activities were observed. Inhibitors or activators of PKC were used to observe the roles of PKC pathways on the AGE-HSA stimulated productions of FN in HPMC.
RESULTSAGE-HSA activated PKC in HPMC in a dose, time-dependent manner (P < 0.05). AGE-HSA up-regulated the expression of FN mRAN and protein in dose- and time-dependently (P < 0.01); PKC activator phorbol 12-myristate 13-acetate (PMA) induced FN expression, respectively depletion of PKC and calphostin C, a PKC inhibitor, effectively prevented both PMA and AGE-HSA-induced expression of the FN (P < 0.05).
CONCLUSIONAGEs can increase the activities of PKC. AGEs can directly increase FN expression in HPMC which may contribute to peritoneal fibrosis and this is regulated by PKC.
