Bufalin inhibits PDGF-BB-induced mesangial cell proliferation via mediating gap junctional intercellular communication.
- Author:
Ying HAN
1
;
Ai-Qing ZHANG
;
Jun ZHANG
;
Jing GONG
;
Shan-Wen LI
;
Wei-Hua GAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bufanolides; pharmacology; Calcium; metabolism; Cell Communication; drug effects; Cell Proliferation; drug effects; Cells, Cultured; Gap Junctions; drug effects; Mesangial Cells; drug effects; physiology; ultrastructure; Proto-Oncogene Proteins c-sis; pharmacology; Rats
- From: Chinese Journal of Contemporary Pediatrics 2012;14(12):982-987
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the role and possible mechanisms of gap junctional intercellular communication (GJIC) involved in mesangial cell (MC) proliferation which could be inhibited by bufalin.
METHODSRat mesangial cells were cultured in vitro. The effect of bufalin on platelet-derived growth factor-BB (PDGF-BB)-induced MC proliferation was evaluated by MTT assay. The function of GJIC was detected by Lucifer Yellow scrape loading and dye transfer (SLDT). mRNA levels of Cx43, Cx45 and Cx40 were measured by RT-PCR. Intracellular calcium concentrations ([Ca(2+)]i) were examined in laser scanning confocal microscopy after loading by Fura-3/AM.
RESULTSMTT indicated that bufalin could inhibited PDGF-BB-induced MC proliferation (P<0.01). Compared with the hormal control group, PDGF-BB inhibited GJIC function, increased the expression of Cx45 and Cx40 (P<0.01) without altering the Cx43 (P>0.05) in gene level and also increased [Ca(2+)]i. However, bufalin treatment enhanced GJIC function, decreased Cx45 mRNA and Cx40 mRNA expression (P<0.01), and reduced [Ca(2+)]i (P<0.01).
CONCLUSIONSBufalin inhibits PDGF-BB-induced MC proliferation, and its possible mechanisms may be related to regulation of Cx45 and Cx40 expression in the gene level, reduction of [Ca(2+)]i and enhancement of GJIC function.
