ABSTRACT
AIM:To explore the effect of Wnt/β-catenin signaling pathway in airway smooth muscle cells (ASMC) on asthmatic airway remodeling.METHODS:The asthmatic airway remodeling model in rats was established and the ASMC was isolated and cultured.The protein expression of β-catenin,glycogen synthase kinase-3β (GSK-3β),cMyc and cyclin D1 in the ASMC was determined by Western blot.After depressing the interaction between β-catenin and p300/CBP,the cell activity was measured by CCK-8 assay and the change of cell cycle distribution was analyzed by flow cytometry.Meanwhile,the protein expression of c-Myc and cyclin D1 in the ASMC was determined by Western blot after inhibiting P38 mitogen-activated protein kinase (MAPK) activity.RESULTS:The protein levels of β-catenin,c-Myc and cyclin D1 were significantly increased in asthma group while the protein level of GSK-3β was decreased in the same group (P ＜ 0.05).After depressing the interaction between β-catenin and p300/CBP,the cell activity of ASMC was decreased in asthma group compared with control group (P ＜ 0.05),and the change of the cell cycle distribution in asthma group was also more obvious (P ＜ 0.05).After inhibiting P38 MAPK activity,the protein levels of c-Myc and cyclin D1 were all decreased compared with control group in ASMC asthma and control rats (P ＜ 0.05).CONCLUSION:Wnt/β-catenin signaling pathway may participates in airway remodeling in asthma by increasing the protein expression of c-Myc and cyclin D1,reacting with the P38 MAPK signaling pathway and regulating the growth of ASMC.
ABSTRACT
AIM:To explore the effect of Wnt/β-catenin signaling pathway in airway smooth muscle cells (ASMC) on asthmatic airway remodeling.METHODS:The asthmatic airway remodeling model in rats was established and the ASMC was isolated and cultured.The protein expression of β-catenin,glycogen synthase kinase-3β (GSK-3β),cMyc and cyclin D1 in the ASMC was determined by Western blot.After depressing the interaction between β-catenin and p300/CBP,the cell activity was measured by CCK-8 assay and the change of cell cycle distribution was analyzed by flow cytometry.Meanwhile,the protein expression of c-Myc and cyclin D1 in the ASMC was determined by Western blot after inhibiting P38 mitogen-activated protein kinase (MAPK) activity.RESULTS:The protein levels of β-catenin,c-Myc and cyclin D1 were significantly increased in asthma group while the protein level of GSK-3β was decreased in the same group (P ＜ 0.05).After depressing the interaction between β-catenin and p300/CBP,the cell activity of ASMC was decreased in asthma group compared with control group (P ＜ 0.05),and the change of the cell cycle distribution in asthma group was also more obvious (P ＜ 0.05).After inhibiting P38 MAPK activity,the protein levels of c-Myc and cyclin D1 were all decreased compared with control group in ASMC asthma and control rats (P ＜ 0.05).CONCLUSION:Wnt/β-catenin signaling pathway may participates in airway remodeling in asthma by increasing the protein expression of c-Myc and cyclin D1,reacting with the P38 MAPK signaling pathway and regulating the growth of ASMC.
ABSTRACT
<p><b>OBJECTIVE</b>To establish Surface-enhanced Raman Spectroscopy (SERS) can be used as a rapid and reliable method to distinguish virulent strain and mild strain of L. pneumophila.</p><p><b>METHODS</b>Mortality data were collected from company departments through administrative documents, death certificates, etc. Trend analyses of cancer mortality were performed on the basis of 925 cancer deaths between 2001 and 2010.</p><p><b>RESULTS</b>Our results indicated that the peaks of high virulence strains reached ⋝4000. This criterion was verified by subsequent cell experiments. In addition, we also conducted SERS rapid identification on the virulence of several collected clinical strains and obtained accurate results.</p><p><b>CONCLUSION</b>The present study indicates that the established SERS protocol can be used as a rapid and reliable method to distinguish virulent and mildly virulent strains of L. pneumophila, which can be further used in clinical samples.</p>