Effect of basic fibroblast growth factor on the proliferation, migration and phenotypic modulation of airway smooth muscle cells.
- Author:
Hui ZOU
1
;
Xiu-hong NIE
;
Yi ZHANG
;
Mu HU
;
Yu Alex ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Actins; analysis; genetics; Bronchi; cytology; drug effects; physiology; Cell Movement; drug effects; Cell Proliferation; drug effects; Cells, Cultured; Fibroblast Growth Factor 2; pharmacology; Humans; Major Histocompatibility Complex; Myocytes, Smooth Muscle; drug effects; Phenotype; RNA, Messenger; analysis
- From: Chinese Medical Journal 2008;121(5):424-429
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDProliferation, cell migration and phenotypic modulation of airway smooth muscle cells (ASMCs) are important features of airway remodelling in asthma. The precise cellular and molecular mechanisms that regulate ASMCs proliferation, migration and phenotypic modulation in the lung remain unknown. Basic fibroblast growth factor (bFGF), a highly specific chemotactic and mitogenic factor for many cell types, appears to be involved in the development of airway remodelling. Our study assessed whether bFGF directly stimulates the proliferation, migration and phenotypic modulation of ASMCs.
METHODSConfluent and growth arrested human ASMCs were treated with human recombinant FGF. Proliferation was measured by BrdU incorporation and cell counting. Migration was examined using Boyden chamber apparatus. Expressions of smooth muscle (sm)-alpha-actin and sm-myosin heavy chain (MHC) isoform 1 were determined by RT-PCR and Western blot analysis.
RESULTSIt was found that hrbFGF (10 ng/ml), when added to ASMCs, induced a significant increase in BrdU uptake and cell number by ASMCs as compared to controls and a significant increase in ASMCs migration with respect to controls. The mRNA and protein expressions of sm-alpha-actin and sm-MHC in ASMCs that were stimulated with hrbFGF decreased with respect to controls.
CONCLUSIONIt appears that bFGF can directly stimulate proliferation and migration of ASMCs, however, the expressions of cells' contractive phenotype decreased.