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Regulation of miRNA expression in the prefrontal cortex by fecal microbiota transplantation in anxiety-like mice

Bibliographic Data

ID15526795
AuthorsSimin Chen (0009-0007-8712-7176, Beijing University of Chinese Medicine), Mengjia Li (0000-0002-0336-5166, Beijing University of Chinese Medicine), Changqing Tong (0009-0002-9587-2110, Beijing University of Chinese Medicine), Yanan Wang (0009-0004-4757-9563, Beijing University of Chinese Medicine), Jiahui He (0000-0003-1004-9679, Beijing University of Chinese Medicine), Qi Shao (0009-0009-0939-8573, Beijing University of Chinese Medicine), Yan Liu (0000-0002-1612-779X, Beijing University of Chinese Medicine, corresponding author), Ying Wu (0000-0002-0016-8052, Fourth Affiliated Hospital of Guangxi Medical University, corresponding author), Yuehan Song (Beijing University of Chinese Medicine, corresponding author)
Year2024
Volume15
Pages1323801-1323801
Publication date2024-02-12
Peer ReviewedYes
Open AccessYes
TypeARTICLE
VenueFrontiers in Psychiatry (JOURNAL)
Journal identifiersISSN: 1664-0640 • E-ISSN: 1664-0640
PublisherFrontiers Media (PUBLISHER • CH)
DOI10.3389/fpsyt.2024.1323801
PMID38410679
OpenAlexW4391750161
LanguageEN
References cited5

This study demonstrates that anxiety-like behavior induced by human FMT can be transmitted through gut microbiota and is associated with miRNA expression in the prefrontal cortex. It is inferred that the reduction of Akkermansia caused by FMT from GAD patients leads to the upregulation of mmu-miR-488-3p expression, resulting in the downregulation of its downstream target gene Creb1 and interference with its related signaling pathway. These findings highlight the gut microbiota's crucial role in the GAD pathophysiology

Anxiety · Biology · Cognition · Fecal bacteriotherapy · microRNA · Prefrontal cortex · Psychiatry · Clinical Psychology · Gastrointestinal motility and disorders · Gut microbiota and health · Medicine · Neuroscience · Psychology · Tryptophan and brain disorders · Genetics · Internal Medicine · Transplantation

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  • MicroRNAs and Gene–Environment Interactions in Autism

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