Journal
CELLULAR AND MOLECULAR NEUROBIOLOGY
Volume 42, Issue 6, Pages 1887-1895Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10571-021-01070-x
Keywords
Traumatic brain injury; Astrocyte; Mitochondria transfer; GJA1-20K; Cx43
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Funding
- Shanghai Natural Science Foundation [19ZR1447400]
- Key Project of Jiangxi Science and Technology Department [20192BBGL70022]
- National Natural Science Foundation of China [81960236]
- Key scientific research projects of Jiangxi Provincial Department of Education [GJJ190022]
- Scientific research plan of Jiangxi health and Family Planning Commission [20203139]
- Younth Key Project of Jiangxi Natural Science Foundation [20202ACBL216005]
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The study revealed that the GJA1-20K/Cx43 axis plays a crucial role in the astrocyte-neuron interaction after simulated TBI, by enhancing functional Cx43 expression in astrocytes and promoting the transmission of mitochondria from astrocytes to neurons, ultimately protecting neurons from damage.
Astrocytes are crucial in neural protection after traumatic brain injury (TBI), a global health problem causing severe brain tissue damage. Astrocytic connexin 43 (Cx43), encoded by GJA1 gene, has been demonstrated to facilitate the protection of astrocytes to neural damage with unclear mechanisms. This study aims to explore the role of GJA1-20K/Cx43 axis in the astrocyte-neuron interaction after TBI and the underlying mechanisms. Primarily cultured cortical neurons isolated from embryonic C57BL/6 mice were treated by compressed nitrogen-oxygen mixed gas to simulate TBI-like damage in vitro. The transwell astrocyte-neuron co-culture system were constructed to recapitulate the interaction between the two cell types. Quantitative PCR was applied to analyze mRNA level of target genes. Western blot and immunofluorescence were conducted to detect target proteins expression. GJA1-20K overexpression significantly down-regulated the expression of phosphorylated Cx43 (p-Cx43) without affecting the total Cx43 protein level. Besides, GJA1-20K overexpression obviously enhanced the dendrite length, as well as the expression levels of function and synthesis-related factors of mitochondria in damaged neurons. GJA1-20K up-regulated functional Cx43 expression in astrocytes, which promoted mitochondria transmission from astrocytes to neurons which might be responsible to the protection of astrocyte to neurons after TBI-like damage in vitro.
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