V-set and immunoglobulin domain containing 4 inhibits oxidative stress, mitochondrial dysfunction, and inflammation to attenuate Parkinson's disease progression by activating the JAK2/STAT3 pathway

• Published in: Journal of neuroimmunology 2024-06, Vol.391, p.578345, Article 578345
• Main Authors: Cai, Pingping, Wang, Junmei, Xu, Jiangtao, Zhang, Min, Yin, Xinxin, He, Shengquan, Zhuang, Jingcong
• Format: Article
• Language: English
• Subjects: Animals; Cell Line; Disease Progression; Inflammation - metabolism; JAK2/STAT3 pathway; Janus Kinase 2 - metabolism; Mice; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondrial dysfunction; Oxidative Stress - drug effects; Oxidative Stress - physiology; Oxidative stress and inflammation; Parkinson Disease - drug therapy; Parkinson Disease - metabolism; Parkinson's disease; Pyrazoles - pharmacology; Pyrimidines - pharmacology; Signal Transduction - drug effects; Signal Transduction - physiology; STAT3 Transcription Factor - metabolism; V-set and immunoglobulin domain containing 4
• ISSN: 0165-5728; 1872-8421; 1872-8421
• DOI: 10.1016/j.jneuroim.2024.578345

V-set and immunoglobulin domain containing 4 (VSIG4) inhibits neurological dysfunction, microglial M1 polarization, and inflammation to participate in the progression of neurological disorders, but evidence regarding Parkinson's disease (PD) is scarce. The present study intended to investigate the engagement of VSIG4 in PD progression, and the potential mechanism. BV-2 cells were treated with 1-Methyl-4-phenylpyridinium (MPP+) to establish PD model. MPP+ treated BV-2 cells were infected with VSIG4 overexpression adenovirus-associated virus (AAV) (oeVSIG4) and negative control AAV (oeNC), and AZD1480 (JAK2 inhibitor) was added to these cells. MPP+ reduced VSIG4 mRNA (P