BCL11b inhibition exerts neuroprotective effects in   Parkinsons Disease models
Parkinson's disease (PD) is the second most common neurodegenerative disease. Its pathogenesis is complex, and neuroinflammation plays a crucial role in it. Through transcriptome sequencing of an acute PD mouse model induced by MPTP, we found that the expression of BCL11b was significantly increased. BCL11b plays important roles in the growth and development of neuronal cells and the immune-inflammatory system. Studies have found that in the MPP+-induced MN9D cell model and the MPTP-induced mouse model, the expression of BCL11b increased in a time-dependent manner. Meanwhile, the inflammatory conditioned medium could induce an upregulation of BCL11b expression in MN9D cells. Inhibiting BCL11b could exert a neuroprotective effect in the inflammatory PD model and reduce the loss of dopaminergic neurons. Mechanistic studies have shown that BCL11b could activate the JAK2/STAT3 pathway, and inhibiting BCL11b could partially prevent the activation of this pathway. In conclusion, BCL11b is involved in the pathological process of PD by activating the JAK2/STAT3 pathway. Inhibiting BCL11b can effectively rescue the loss of dopaminergic neurons and exert a neuroprotective effect.