Endothelin-1, over-expressed in SOD1G93A mice, aggravates injury of NSC34-hSOD1G93A cells through complicated molecular mechanism revealed by quantitative proteomics analysis

Using proteomic analysis, we revealed that 110 proteins were differentially expressed in NSC34-hSOD1G93A cells after ET-1 treatment in our experiments, of which 54 were up-regulated and 56 were down-regulated. Bioinformatics analysis showed that the differentially expressed proteins (DEPs) were primarily enriched in hippo signaling pathway-multiple species, ABC transporters, ErbB signaling pathway and so on. These results provide further insights on the potential roles of ET-1 in ALS. Our study presents a new promising therapeutic target to protect MNs of ALS.