Abstract:
BACKGROUND:Although it is recognized that bronchial smooth muscle cells (BSMCs) play a key role in airway remodeling during chronic asthma, it is not well understood how BSMCs exert their inflammatory functions. The extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is an important signaling pathway in chronic asthma, but its influence on secretion by BSMCs has not been well-studied. We investigated the impact of ERK1/2 signaling pathway on secretion by BSMCs in a rat model of chronic asthma in this study. METHODS:To create a rat model of chronic asthma, Wistar rats underwent ovalbumim (OVA) injection and eight weeks of inhalation. BSMCs were isolated and cultured in vitro. Epidermal growth factor, PD98059 and ERK1/2 antisense oligonucleotide were used to explore the role of ERK1/2 signaling pathway. The expression of P-ERK1/2 (phospho-ERK1/2) in BSMCs was analyzed by Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR). Secretion of BSMCs was detected by enzyme-linked immunosorbent assay (ELISA). RESULTS:Phospho-ERK1/2 expression was increased in BSMCs of chronic asthmatic rats compared with the controls. PD98059 inhibited expression of phospho-ERK1/2 protein, while treatment with an antisense oligonucleotide inhibited the expression of P-ERK1/2 mRNA and protein. BSMCs obtained from the chronic asthma group secreted significantly greater quantities of growth factors (transforming growth factor (TGF)-beta(1), vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF)), cytokines (regulated upon activation, normal T cell-expressed and secreted (RANTES) and eotaxin), and extracellular matrix (fibronectin and collagen I) compared with normal controls. Epidermal growth factor stimulated secretion in both groups, but the response of the chronic asthma group was more intense. Both PD98059 and antisense oligonucleotide suppressed secretion by BSMCs in chronic ashmatic rats. Antisense oligonucleotide reduced the level of RANTES nearly to that of normal controls, while PD98059 could not. CONCLUSION:These results suggest that ERK1/2 signaling pathway may play an important role in the augmented secretion of BSMCs in chronic asthmatic rats, and ERK1/2 antisense oligonucleotide effectively inhibits the process.
journal_name
Chin Med J (Engl)journal_title
Chinese medical journalauthors
Xie M,Liu XS,Xu YJ,Zhang ZX,Bai J,Ni W,Chen SXsubject
Has Abstractpub_date
2008-01-05 00:00:00pages
73-7issue
1eissn
0366-6999issn
2542-5641journal_volume
121pub_type
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journal_title:Chinese medical journal
pub_type: 杂志文章
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journal_title:Chinese medical journal
pub_type: 杂志文章
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journal_title:Chinese medical journal
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pub_type: 杂志文章,评审
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pub_type: 杂志文章
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pub_type: 杂志文章,多中心研究,随机对照试验
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pub_type: 杂志文章
doi:
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pub_type: 杂志文章
doi:10.4103/0366-6999.156784
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pub_type: 临床试验,杂志文章,随机对照试验
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journal_title:Chinese medical journal
pub_type: 杂志文章,多中心研究
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doi:
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journal_title:Chinese medical journal
pub_type: 杂志文章,meta分析,评审
doi:
更新日期:2004-03-01 00:00:00
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journal_title:Chinese medical journal
pub_type: 杂志文章
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journal_title:Chinese medical journal
pub_type: 杂志文章
doi:
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journal_title:Chinese medical journal
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journal_title:Chinese medical journal
pub_type: 杂志文章
doi:
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pub_type: 杂志文章
doi:
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doi:
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