Expression and Significance of protein 4.1R in rat models with diaphragmatic weakness

Abstract Abstract Background To explore the significance of protein 4.1R expression in the diaphragmatic weakness animal and cell models and its preliminary mechanism. Methods Rats were intraperitoneally injected with Lipopolysaccharide (LPS) to construct diaphragmatic weakness models. Histopathology of diaphragmatic tissues was detected by Hematoxylin eosin(HE) staining. L6 cells were induced by LPS to establish the myasthenic cell models and transfected with 4.1R-siRNA to konckdown 4.1R. Immunohistochemistry was performed to detect the expression of acetylcholine receptor(AchR) and 4.1R; The expression of desmin and myosin in tissues and cells were detected by western blot. Results LPS could induce the diaphragmatic weakness of rats. The expression of AchR in diaphragmatic weakness tissues was lower, while that of desmin was higher than that in the control group. 4.1R was up-regulated in the diaphragmatic weakness models, and related to the severity. After knockdown of 4.1R in LPS induced L6 cells, the expression of AchR was up-regulated significantly. But there was not difference of contractile proteins. Conclusions Protein 4.1R was upregulated in diaphragmatic weakness model in vivo and in vitro and might be involved into the occurrence of myasthenia gravis by negatively regulating the expression of AchR.