Open AccessMicroRNA‐345‐5p regulates depression by targeting suppressor of cytokine signaling 1
Author(s) -
Liu Yulan,
Yu Jun,
Wang Xinrui,
Dong Jicheng
Publication year - 2020
Publication title -
brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.915
H-Index - 41
ISSN - 2162-3279
DOI - 10.1002/brb3.1653
Subject(s) - microglia , viability assay , microrna , suppressor of cytokine signaling 1 , western blot , hippocampal formation , microbiology and biotechnology , apoptosis , flow cytometry , biology , cytokine , neuroinflammation , chemistry , immunology , inflammation , neuroscience , suppressor , gene , biochemistry
Abstract Background/Aims MicroRNA(miR)‐345‐5p plays a key role in various cellular functions. However, the function of miR‐345‐5p in resistant depression (TRD) is unclear. The aim of this study was to evaluate the role and mechanism of miR‐345‐5p in the treatment of resistance depression (TRD). Methods RT‐qPCR was used to detect the expression of miR‐345‐5p in BV‐2 microglia. CCK‐8 method and flow cytometry were used for cell viability and apoptosis of microglia. Target gene prediction and screening, and luciferase reporter assays were used to verify the downstream target gene of miR‐345‐5p. Western blot was used to analyze the protein expression of related proteins. Results miR‐345‐5p increased the cell viability of BV‐2 microglia and the expression level of pro‐inflammatory cytokines. In addition, the conditioned medium of microglia treated with miR‐345‐5p reduced the cell viability of HT22 hippocampal cells and caused S‐phase arrest. The miR‐345‐5p‐treated microglia induced apoptosis by regulating the expression levels of Bax, Bcl‐2, pro‐caspase‐3, and cleaved caspase‐3. Furthermore, SOCS1 was a direct target of miR‐345‐5p, and overexpression of SOCS1 was able to reverse the proapoptotic effect of miR‐345‐5p on activation of microglia on hippocampal neurons. Conclusion miR‐345‐5p induced inflammatory damage in hippocampal neurons by activating microglia. MiR‐345‐5p may be an effective target for TRD therapy.