Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: The effect of substance P on asthmatic rat airway smooth muscle cell proliferation, migration, and cytoplasmic calcium concentration in vitro. | Li et al. Journal of Inflammation 2011 8 18 http content 8 1 18 JOURNAL OF INFLAMMATION RESEARCH Open Access The effect of substance P on asthmatic rat airway smooth muscle cell proliferation migration and cytoplasmic calcium concentration in vitro Miao Li Yun-Xiao Shang Bing Wei and Yun-Gang Yang Abstract Airway remodeling and airway hyper-responsiveness are prominent features of asthma. Neurogenic inflammation participates in the development of asthma. Neurokinin substance P acts by binding to neurokinin-1 receptor NK-1R . Airway smooth muscle cells ASMC are important effector cells in asthma. Increases in ASMC proliferation migration and cytoplasmic Ca2 concentration are critical to airway remodeling and hyper-responsiveness. The effects of substance P on ASMC were investigated in Wistar rats challenged with a previously described asthmatic rat model. To exclude possible influences from other factors the role of substance P was also investigated in primary cultured rat ASMC. Substance P and WIN62577-induced changes in cytoplasmic Ca2 concentration were observed by fluorescence microscopy and expression of Ca2 homeostasis-regulating genes was assessed with real-time PCR. We found that cytoplasmic Ca2 concentration increased in normal rat ASMC treated with substance P but decreased in asthmatic rat ASMC treated with WIN62577 an antagonist of NK-1R. Real-time PCR analysis revealed increased Serca2 mRNA expression but decreased Ip3r mRNA expression after WIN62577 treatment in asthmatic rat ASMC. Flow cytometric analysis FCM revealed that most asthmatic rat ASMC stayed at G1 phase after combined treatment with WIN62577 and IL-13 in vitro. Transwell analysis suggested that ASMC migration was reduced after WIN62577 treatment. Therefore we conclude that NK-1R is related to asthma mechanisms and a NK-1R antagonist downregulates calcium concentration in asthmatic ASMC by increasing Serca2 mRNA and decreasing Ip3r mRNA expression. The NK-1R .
