Phosphoinositide 3-kinases promotes proliferation of airway smooth muscle cells in asthmatic rats
Chunsheng Fang
Abstract
Chunsheng Fang
Abstract
Objective To explore the effect of Phosphoinositide 3-Kinases(PI3K) in airway remodeling in asthmatic rats.Methods Twenty-four rats were randomly divided into control group,asthmatic 4 weeks group and 6 weeks group(n=8).The airway resistance and eosinophilic inflammation of airway wall were observed;the airway wall thickness(WA/Pi),the bronchial smooth muscle thickness(smooth muscle area/Pi) and the number of bronchial smooth muscle nucleus(N/Pi) were measured by image analysis system;the expression of PI3K protein and mRNA were determined by immunohistochemical staining and reverse transcription-polymerase chain reaction(RT-PCR).Results(1) The expression of PI3K P85α was mainly located in the rat airway epithelial cells and airway smooth muscle cells.The expression of PI3K P85α protein and mRNA in two asthmatic groups was significantly higher than control group,respectively(P0.01),and in asthmatic 6 weeks group was higher than asthmatic 4 weeks group,respectively(P0.05,P0.01).(2) The airway wall thickness,bronchial smooth muscle thickness and the number of bronchial smooth muscle nucleus in two asthmatic groups were significantly higher than control group,respectively(P0.01),and in asthmatic 6 weeks group were higher than asthmatic 4 weeks group,respectively(P0.01).(3) The airway resistance in two asthmatic groups were significantly higher than control group,respectively(P0.01),and in asthmatic 6 weeks group were higher than asthmatic 4 weeks group,respectively(P0.05).Conclusion The PI3K signal pathway may be involved in AHR and the airway remodeling through promoting airway smooth muscle cells proliferation in asthma.
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Objective To explore the effect of Phosphoinositide 3-Kinases(PI3K) in airway remodeling in asthmatic rats.Methods Twenty-four rats were randomly divided into control group,asthmatic 4 weeks group and 6 weeks group(n=8).The airway resistance and eosinophilic inflammation of airway wall were observed;the airway wall thickness(WA/Pi),the bronchial smooth muscle thickness(smooth muscle area/Pi) and the number of bronchial smooth muscle nucleus(N/Pi) were measured by image analysis system;the expression of PI3K protein and mRNA were determined by immunohistochemical staining and reverse transcription-polymerase chain reaction(RT-PCR).Results(1) The expression of PI3K P85α was mainly located in the rat airway epithelial cells and airway smooth muscle cells.The expression of PI3K P85α protein and mRNA in two asthmatic groups was significantly higher than control group,respectively(P0.01),and in asthmatic 6 weeks group was higher than asthmatic 4 weeks group,respectively(P0.05,P0.01).(2) The airway wall thickness,bronchial smooth muscle thickness and the number of bronchial smooth muscle nucleus in two asthmatic groups were significantly higher than control group,respectively(P0.01),and in asthmatic 6 weeks group were higher than asthmatic 4 weeks group,respectively(P0.01).(3) The airway resistance in two asthmatic groups were significantly higher than control group,respectively(P0.01),and in asthmatic 6 weeks group were higher than asthmatic 4 weeks group,respectively(P0.05).Conclusion The PI3K signal pathway may be involved in AHR and the airway remodeling through promoting airway smooth muscle cells proliferation in asthma.
Key concepts: Airway, Medicine, Immunohistochemistry, Asthma, Phosphoinositide 3-kinase, Messenger RNA, Kinase, Airway resistance