Astrocyte-derived exosome-transported GJA1-20k attenuates traumatic brain injury in rats

作者：Jiugeng Feng, Shufeng Zou, Xuanyong Yang, Zhigang Wang, Bixia Jiang, Tingting Hou, Jian Duan, Tao Hong, Wei Chen · 发表于：Chinese Medical Journal · 年份：2022 · DOI：10.1097/cm9.0000000000002320 · 被引用次数：10 · 研究领域：Connexins and lens biology、Extracellular vesicles in disease、Traumatic Brain Injury and Neurovascular Disturbances

To the Editor: Traumatic brain injury (TBI) refers to brain tissue damage caused by trauma. TBI pathogenesis is complicated and the involved molecular targets are also not clear. Astrocytes proliferate and hypertrophy after brain injury. They have strong tolerance to hypoxia and ischemia to protect neurons in the acute phase of brain injury. Exosomes, as small vesicles to exchange material and transmit information between cells, have been reported to exhibit potentials against various impairments in different disease models, including neurological diseases.[1] One recent study has shown that exosomes are closely related to trauma, which may decrease A1 astrocytes by down-regulation of phosphorylation of nuclear factor-kappa B (NF-κB) in spinal cord injury.[2] Our previous study demonstrated that the TBI could promote exosome release, suggesting the capability of self-protection by exosomes after impairment.[3] Connexin 43 (Cx43, also called gap junction alpha 1 [GJA1]) is an important gap junction protein with widest expression.[4] GJA1-20k is a non-classical Cx43 protein with a fully truncated N-terminal. Our previous study showed that GJA1-20k overexpression in astrocytes promoted the recovery and viability of neurons in TBI by regulating mitochondrial function.[5] Herein, the present study aimed to explore the protective effects of exosomes from GJA1-20k overexpressed astrocytes on TBI. Exosomes were isolated from astrocytes transducted with lentiviral vector GJA1-20k, def...