Effect of transforming growth factor β_1 on the activity of extracellular signal-regulated kinase1/2 of airway smooth muscle cells in different periods of asthmatic rats
Zhang Huan-pin
Abstract
Zhang Huan-pin
Abstract
Objective To investigate the effect of transforming growth factor β1(TGF-β1) on airway smooth muscle cells (ASMC) expression of extracellular signal-regulated kinase (ERK)1/2 mRNA and phosphorylated forms of ERK1/2(p-ERK1/2) in different periods asthmatic rats.Methods The establishment of 2W,6W rat model of asthma through ovalbumin (OVA) sensitization and excitation.TGF-β1 and ERK inhibitor PD98059 were used in the cell culture.The expressions of ERK1/2 mRNA were detected by RT-PCR,the location and protein expressions of p-ERK1/2 were examined by immunocytochemical staining.Results The results showed that in 2W,6W asthmatic groups,compared with that in the control group,the expressions of ERK mRNA,p-ERK1/2 protein and the activation ratio of ERK in ASMC in asthmatic groups were significantly increased compared with those in the control group.After treatment with PD98059,the expressions of ERK mRNA,p-ERK1/2 protein and the activation ratio of ERK in ASMC in asthmatic groups were significantly decreased compared with those in the control group.After treatment with group TGF-β1,the expressions of ERK mRNA,p-ERK1/2 protein and the activation ratio of ERK in ASMC in 2W and 6W asthmatic group were significantly decreased compared with those in their asthmatic group.And this role can be partly inhibited by PD98059.There is no difference between the 2W and 6W asthmatic model group with these results.Conclusions TGF-β1 up-regulated expression of ERK1/2 mRNA and p-ERK1/2 in different periods asthmatic rats,at different stages of asthma,TGF-β1 is likely to continue through the promotion of ERK signal transduction pathway of the activity on the proliferation of ASMC regulate.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To investigate the effect of transforming growth factor β1(TGF-β1) on airway smooth muscle cells (ASMC) expression of extracellular signal-regulated kinase (ERK)1/2 mRNA and phosphorylated forms of ERK1/2(p-ERK1/2) in different periods asthmatic rats.Methods The establishment of 2W,6W rat model of asthma through ovalbumin (OVA) sensitization and excitation.TGF-β1 and ERK inhibitor PD98059 were used in the cell culture.The expressions of ERK1/2 mRNA were detected by RT-PCR,the location and protein expressions of p-ERK1/2 were examined by immunocytochemical staining.Results The results showed that in 2W,6W asthmatic groups,compared with that in the control group,the expressions of ERK mRNA,p-ERK1/2 protein and the activation ratio of ERK in ASMC in asthmatic groups were significantly increased compared with those in the control group.After treatment with PD98059,the expressions of ERK mRNA,p-ERK1/2 protein and the activation ratio of ERK in ASMC in asthmatic groups were significantly decreased compared with those in the control group.After treatment with group TGF-β1,the expressions of ERK mRNA,p-ERK1/2 protein and the activation ratio of ERK in ASMC in 2W and 6W asthmatic group were significantly decreased compared with those in their asthmatic group.And this role can be partly inhibited by PD98059.There is no difference between the 2W and 6W asthmatic model group with these results.Conclusions TGF-β1 up-regulated expression of ERK1/2 mRNA and p-ERK1/2 in different periods asthmatic rats,at different stages of asthma,TGF-β1 is likely to continue through the promotion of ERK signal transduction pathway of the activity on the proliferation of ASMC regulate.
Key concepts: MAPK/ERK pathway, Ovalbumin, Kinase, Medicine, Extracellular, Messenger RNA, Transforming growth factor, Internal medicine