Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: " Reverse mode Na+/Ca2+ exchange mediated by STIM1 contributes to Ca2+ influx in airway smooth muscle following agonist stimulation. | Liu et al. Respiratory Research 2010 11 168 http content 11 1 168 RESPIRATORY RESEARCH RESEARCH Open Access Reverse mode Na Ca2 exchange mediated by STIM1 contributes to Ca2 influx in airway smooth muscle following agonist stimulation Bo Liu Samantha E Peel Jane Fox Ian P Hall Abstract Background Agonist stimulation of airway smooth muscle ASM results in IP3 mediated Ca2 release from the sarcoplasmic reticulum followed by the activation of store operated and receptor operated non-selective cation channels. Activation of these non-selective channels also results in a Na influx. This localised increase in Na levels can potentially switch the Na Ca2 exchanger into reverse mode and so result in a further influx of Ca2 . The aim of this study was to characterise the expression and physiological function of the Na Ca2 exchanger in cultured human bronchial smooth muscle cells and determine its contribution to agonist induced Ca2 influx into these cells. Methods The expression profile of NCX which encodes the Na Ca2 exchanger homologues in cultured human bronchial smooth muscle cells was determined by reverse transcriptase PCR. The functional activity of reverse mode NCX was investigated using a combination of whole cell patch clamp intracellular Ca2 measurements and porcine airway contractile analyses. KB-R7943 an antagonist for reverse mode NCX and target specific siRNA were utilised as tools to inhibit NCX function. Results NCX1 protein was detected in cultured human bronchial smooth muscle cells HBSMC cells and was the only mRNA transcript variant detected. A combination of intracellular Na loading and addition of extracellular Ca2 induced an outwardly rectifying current which was augmented following stimulation with histamine. This outwardly rectifying current was inhibited by 10 pM KB-R7943 an antagonist of reverse mode NCX1 and was reduced in cells incubated with siRNA against NCX1. Interestingly this outwardly rectifying current was
