The autophagy protein ATG8 inhibited the formation of endometriosis by regulating Treg cells differentiation via mediating the interaction between integrin α4β1 and Talin-1

Research Question Endometriosis (EMS) is a common chronic inflammatory gynecological disease. The research intends to explore the relationship between ATG8 and integrin α4β1, Talin-1, and Treg cell differentiation and the effects on EMS. Design First, the clinical correlation between the ATG8, Talin-1, integrin α4β1, and differentiation of Treg cells and EMS was examined in clinical samples. Human PBMCs and ESCs were extracted and identified, the oe-ATG8 and oe-integrin α4β1 were transfected, and Tregs cell differentiation and ESCs function were detected. In addition, we investigated the molecular mechanism by which ATG8 inhibited EMS disease progression at the molecular and animal levels. Results ATG8 expression was negatively correlated with Talin-1 and integrin-α4β1 levels, and positive proportion of Tregs cells, respectively. The expression of Talin-1 and integrin-α4β1 in PBMCs decreased significantly after oe-ATG8 transfection, while the Treg cells' positive rate significantly increased. The ESCs proliferation, adhesion, migration, and invasion declined after co-cultured with Treg cells that oe-ATG8 transfection. The expression of Talin-1 and integrin-α4β1 in PBMCs decreased significantly after oe-integrin α4β1 transfection. In addition, oe-integrin α4β1 transfection reversed the corresponding regulation of oe-ATG8 transfection. Finally, animal experiments in vivo confirmed that ATG8 inhibited EMS disease progression. Conclusion The ATG8 regulated Treg cell differentiation and inhibited EMS formation by influencing the interaction between integrin α4β1 and Talin-1.