Lanthanum Chloride Induces Axon Abnormality Through LKB1-MARK2 and LKB1-STK25-GM130 Signaling Pathways

Abstract

Lanthanum (La) is a natural rare-earth element that can damage the central nervous system and impair learning and memory. However, its neurotoxic mechanism remains unclear. In this study, adult female rats were divided into 4 groups and given distilled water solution containing 0%, 0.125%, 0.25%, and 0.5% LaCl₃, respectively, and this was done from conception to the end of the location. Their offspring rats were used to establish animal models to investigate LaCl₃ neurotoxicity. Primary neurons cultured in vitro were treated with LaCl₃ and infected with LKB1 overexpression lentivirus. The results showed that LaCl₃ exposure resulted in abnormal axons in the hippocampus and primary cultured neurons. LaCl₃ reduced the expression of LKB1, p-LKB1, STRAD and MO25 proteins, and directly or indirectly affected the expression of LKB1, leading to decreased activity of LKB1-MARK2 and LKB1-STK25-GM130 pathways. This study indicated that LaCl₃ exposure could interfere with the normal effects of LKB1 in the brain and downregulate LKB1-MARK2 and LKB1-STK25-GM130 signaling pathways, resulting in abnormal axon in offspring rats.

Keywords: Axon; LKB1; Lanthanum; Learning and memory.