摘要
Background Proliferation, 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. Methods Confluent 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）-α-actin and sm-myosin heavy chain （MHC） isoform 1 were determined by RT-PCR and Westem blot analysis. Results It 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-α-actin and sm-MHC in ASMCs that were stimulated with hrbFGF decreased with respect to controls. Conclusion It appears that bFGF can directly stimulate proliferation and migration of ASMCs, however, the expressions of cells＇ contractive phenotype decreased.
Background Proliferation, 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. Methods Confluent 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）-α-actin and sm-myosin heavy chain （MHC） isoform 1 were determined by RT-PCR and Westem blot analysis. Results It 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-α-actin and sm-MHC in ASMCs that were stimulated with hrbFGF decreased with respect to controls. Conclusion It appears that bFGF can directly stimulate proliferation and migration of ASMCs, however, the expressions of cells＇ contractive phenotype decreased.
