神经毒性
星形胶质细胞
内化
神经退行性变
细胞生物学
邻苯二甲酸盐
神经炎症
胶质纤维酸性蛋白
自噬
生物
化学
神经科学
中枢神经系统
生物化学
毒性
免疫学
医学
病理
细胞
免疫组织化学
炎症
细胞凋亡
有机化学
疾病
作者
Yingxin Zhao,Yi-Xi Tang,Xuxu Sun,Shi‐Yong Zhu,Xueyan Dai,Xuenan Li,Jin-Long Li
标识
DOI:10.1021/acs.jafc.2c01635
摘要
Di-(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer in plastic products, consumer products, and packaging materials. It is of great health concern in both animals and humans as it released into the environment and entered into the body from plastic products over time, thereby resulting in neurotoxicity. As a pivotal regulator of the central nervous system (CNS), astrocytes, are crucial for maintaining brain homeostasis. Nevertheless, the underlying reason for astrocyte neurotoxicity due to DEHP exposure remains incompletely understood. Here, using an in vivo model of neurotoxicity in quail, this study summarizes that Cx43 is internalized by phosphorylation and translocated to the nucleus as a consequence of DEHP exposure in astrocytes. This study further demonstrated that astrocytes transformed to pro-inflammatory status and induced the formation of autophagosomes. Of note, integrated immunofluorescent codetection approaches revealed an overexpression of the glial fibrillary acidic protein (GFAP) and down-expression of Cx43 in astrocytes. Therefore, in terms of neurotoxicity, this experiment in vivo models directly linked Cx43 internalization to autophagy and neuroinflammation and ultimately locked these changes to the astrocytes of the brain. These findings unveil a potential approach targeting Cx43 internalization for the treatment of neurodegeneration caused by DEHP exposure in astrocytes.
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