细胞生长
血小板源性生长因子受体
内分泌学
细胞因子
MAPK/ERK通路
内科学
血小板衍生生长因子
生物
转化生长因子
生长因子
肿瘤坏死因子α
细胞生物学
免疫学
信号转导
医学
受体
生物化学
作者
Rodopi Stamatiou,Efrosyni Paraskeva,K. Gourgoulianis,Paschalis‐Adam Molyvdas,Apostolia Hatziefthimiou
出处
期刊:ISRN Inflammation (Online)
[Hindawi Limited]
日期:2012-07-08
卷期号:2012: 1-13
被引量:26
摘要
Chronic airway diseases, such as asthma or chronic obstructive pulmonary disease, are characterized by the presence in the airways of inflammation factors, growth factors and cytokines, which promote airway wall remodelling. The aim of this study was to investigate the effect of cytokines and growth factors on airway smooth muscle cell (ASMC) proliferation, phenotype and responsiveness. Incubation of serum starved human bronchial ASMCs with TNF- α , TGF, bFGF, and PDGF, but not IL-1 β , increased methyl-[(3)H]thymidine incorporation and cell number, mediated by the PI3K and MAPK signalling pathways. Regarding rabbit tracheal ASMC proliferation, TNF- α , IL-1 β , TGF, and PDGF increased methyl-[(3)H]thymidine incorporation in a PI3K- and MAPK-dependent manner. bFGF increased both methyl-[(3)H]thymidine incorporation and cell number. Moreover, incubation with TGF, bFGF and PDGF appears to drive human ASMCs towards a synthetic phenotype, as shown by the reduction of the percentage of cells expressing SM- α actin. In addition, the responsiveness of epithelium-denuded rabbit tracheal strips to carbachol was not significantly altered after 3-day treatment with bFGF. In conclusion, all the tested cytokines and growth factors increased ASMC proliferation to a different degree, depending on the specific cell type, with bronchial ASMCs being more prone to proliferation than tracheal ASMCs.
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