Journal
CELL CYCLE
Volume 17, Issue 24, Pages 2745-2755Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2018.1556060
Keywords
Major depressive disorder; miR-221; Wnt2/CREB/BDNF
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Funding
- National Natural Science Foundation of China [81571318, 81401110]
- Health and Family Planning Commission of Henan Province [201501015]
- Department of Science and Technology of Henan Province [162102410061, 2017JQ023]
- School and Hospital Co-Incubation Funds [2017-BSTDJJ-04]
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Objective: The aim of this study was to investigate the mechanism of miR-221 in depression. Methods: The molecules expressions were measured by qRT-PCR and western blot. The sucrose preference test (SPT), forced swimming test (FST) and tail suspension test (TST) were used to detect depressive-like symptoms. MTT assay and flow cytometric was used to measure the proliferation and apoptosis of hippocampal neuronal. Results: MiR-221 expression in the cerebrospinal fluid and serum of major depressive disorder patients and the hippocampus of chronic unpredictable mild stress (CUMS) mice were increased, while the expression of Wnt2, p-CREB and BDNF were decreased. Additionally, silence of miR-221 increased sucrose preference of CUMS mice and shortened the immobility time of CUMS mice in SPT and FST. MiR-221 could targeted regulate Wnt2, and knockdown of Wnt2 reversed the effect of miR-221 inhibitor on the proliferation and apoptosis of hippocampal neurons and countered the promoting effect of miR-221 inhibitor on the expression of Wnt2, p-CREB and BDNF. Conclusion: MiR-221 could promote the development of depression by regulating Wnt2/CREB/BDNF axis.
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