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ERK1/2 Signalling Pathway Regulates Tubulin-Binding Cofactor B Expression and Affects Astrocyte Process Formation after Acute Foetal Alcohol Exposure

1
Institute of Neuroscience, Chongqing Medical University, Chongqing 400016, China
2
Institute for Viral Hepatitis, Second Affiliated Hospital of Chongqing Medical University, Chongqing 400063, China
3
Department of Blood Transfusion, Sichuan Cancer Hospital & Institute, Chengdu 610044, China
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editors: Masaru Tanaka, Lydia Giménez-Llort, Simone Battaglia, Chong Chen, Piril Hepsomali and Mark Burke
Brain Sci. 2022, 12(7), 813; https://doi.org/10.3390/brainsci12070813
Received: 23 April 2022 / Revised: 17 June 2022 / Accepted: 20 June 2022 / Published: 22 June 2022
Foetal alcohol spectrum disorders (FASDs) are a spectrum of neurological disorders whose neurological symptoms, besides the neuronal damage caused by alcohol, may also be associated with neuroglial damage. Tubulin-binding cofactor B (TBCB) may be involved in the pathogenesis of FASD. To understand the mechanism and provide new insights into the pathogenesis of FASD, acute foetal alcohol exposure model on astrocytes was established and the interference experiments were carried out. First, after alcohol exposure, the nascent astrocyte processes were reduced or lost, accompanied by the absence of TBCB expression and the disruption of microtubules (MTs) in processes. Subsequently, TBCB was silenced with siRNA. It was severely reduced or lost in nascent astrocyte processes, with a dramatic reduction in astrocyte processes, indicating that TBCB plays a vital role in astrocyte process formation. Finally, the regulating mechanism was studied and it was found that the extracellular signal-regulated protease 1/2 (ERK1/2) signalling pathway was one of the main pathways regulating TBCB expression in astrocytes after alcohol injury. In summary, after acute foetal alcohol exposure, the decreased TBCB in nascent astrocyte processes, regulated by the ERK1/2 signalling pathway, was the main factor leading to the disorder of astrocyte process formation, which could contribute to the neurological symptoms of FASD. View Full-Text
Keywords: tubulin-binding cofactor B; astrocyte processes; microtubules; extracellular signal-regulated protease 1/2 signalling pathway; foetal alcohol spectrum disorders; acute foetal alcohol exposure tubulin-binding cofactor B; astrocyte processes; microtubules; extracellular signal-regulated protease 1/2 signalling pathway; foetal alcohol spectrum disorders; acute foetal alcohol exposure
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MDPI and ACS Style

Zheng, Y.; Huo, J.; Yang, M.; Zhang, G.; Wan, S.; Chen, X.; Zhang, B.; Liu, H. ERK1/2 Signalling Pathway Regulates Tubulin-Binding Cofactor B Expression and Affects Astrocyte Process Formation after Acute Foetal Alcohol Exposure. Brain Sci. 2022, 12, 813. https://doi.org/10.3390/brainsci12070813

AMA Style

Zheng Y, Huo J, Yang M, Zhang G, Wan S, Chen X, Zhang B, Liu H. ERK1/2 Signalling Pathway Regulates Tubulin-Binding Cofactor B Expression and Affects Astrocyte Process Formation after Acute Foetal Alcohol Exposure. Brain Sciences. 2022; 12(7):813. https://doi.org/10.3390/brainsci12070813

Chicago/Turabian Style

Zheng, Yin, Jiechao Huo, Mei Yang, Gaoli Zhang, Shanshan Wan, Xiaoqiao Chen, Bingqiu Zhang, and Hui Liu. 2022. "ERK1/2 Signalling Pathway Regulates Tubulin-Binding Cofactor B Expression and Affects Astrocyte Process Formation after Acute Foetal Alcohol Exposure" Brain Sciences 12, no. 7: 813. https://doi.org/10.3390/brainsci12070813

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