Neuron navigator 2 is a novel mediator of rheumatoid arthritis
Ran Wang, Meng Li, Qian Ding, Jianghong Cai, Yue Yu, Xinhua Liu, Jianchun Mao, Yi Zhun Zhu
Abstract
Rheumatoid arthritis (RA) is a systemic autoimmune disease mainly characterized by synovial tumor-like hyperplasia, synovial inflammation, and damage to adjacent cartilage and bones. 1 Our previous study provided evidence that cystathionine-γ-lyase (CSE) and the histone demethylase JMJD3 are significantly increased in RA, and CSE was found to negatively regulate the inflammatory response in fibroblast-like synoviocytes (FLSs), which was mainly attributed to JMJD3 inhibition, in RA. 2 Our recent data provided further novel insight into the molecular mechanism by which the inflammatory response is regulated in RA pathogenesis. As a member of the neuron navigator (NAV) family, NAV2 was reported to be associated with deeper invasion and lymph node and distant metastases in colorectal carcinoma. 3 Our latest study provides evidence that NAV2 expression is clearly higher in RA patients. TNF-α intervention can significantly increase the level of NAV2, promote proliferation and invasion and further trigger the Wnt/β-catenin signaling pathway. Neutralization or elimination of NAV2 expression may significantly ameliorate RA severity or suppress the development of autoimmune disorders. 4