Background Atrial fibrillation （AF） is the most common sustained cardiac arrhythmia without effective treatment. AF is associated with atrial conduction disturbances caused by electrical and / or structural remodeli...Background Atrial fibrillation （AF） is the most common sustained cardiac arrhythmia without effective treatment. AF is associated with atrial conduction disturbances caused by electrical and / or structural remodeling. But the role of connexin （Cx） 43 in the regulation of L type calcium channel （LCC） remains unclear. We hypothesized that Cx 43 might co-localize and regulate the L type calcium channel current （ICa, D. Methods Real-time PCR and whole-cell patch clamp were used to detect the expression of LCC lc subunit and the cur rent density of Ica, L, before and after Cx 43 knocking down respectively. The co-localization of Cx 43 with LCC was investigated by co-immunoprecipitation and confocal microscopy. Results Knocking down of Cx43 significantly inhibited the current density of ICa, L through decreasing the gene expression of LCC alc in cul tured atrium-derived myocytes （HL-1 cells）. Cx43 co-localized with LCC eric subunit in atrial myocytes. Conclusions Cx 43 regulates the ICa, L in atrial myoctyes through LCC, representing a potential pathogenic mechanism in atrial arrhythmias.展开更多
基金supported by National Natural Science Foundation of China(No.81470440)Guangdong Natural Science Foundation(No.S2013010016256)Medical Scientific Research Foundation of Guangdong Province(No.A2013049)
文摘Background Atrial fibrillation （AF） is the most common sustained cardiac arrhythmia without effective treatment. AF is associated with atrial conduction disturbances caused by electrical and / or structural remodeling. But the role of connexin （Cx） 43 in the regulation of L type calcium channel （LCC） remains unclear. We hypothesized that Cx 43 might co-localize and regulate the L type calcium channel current （ICa, D. Methods Real-time PCR and whole-cell patch clamp were used to detect the expression of LCC lc subunit and the cur rent density of Ica, L, before and after Cx 43 knocking down respectively. The co-localization of Cx 43 with LCC was investigated by co-immunoprecipitation and confocal microscopy. Results Knocking down of Cx43 significantly inhibited the current density of ICa, L through decreasing the gene expression of LCC alc in cul tured atrium-derived myocytes （HL-1 cells）. Cx43 co-localized with LCC eric subunit in atrial myocytes. Conclusions Cx 43 regulates the ICa, L in atrial myoctyes through LCC, representing a potential pathogenic mechanism in atrial arrhythmias.
