Nan Lian1,2,3, Qihui Niu1,2,3, Yang Lei1,2,3, Xue Li1,2,3, Youhui Li1,2,3, Xueqin Song1,2,3. 1. a Department of Psychiatry , The First Affiliated Hospital of Zhengzhou University , Zhengzhou Henan , China. 2. b Biological Psychiatry International Joint Laboratory of Henan , Zhengzhou University , Zhengzhou Henan , China. 3. c Henan Psychiatric Transformation Research Key Laboratory , Zhengzhou University , Zhengzhou Henan , China.
Abstract
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.
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 disorderpatients 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.
Entities:
Keywords:
Major depressive disorder; Wnt2/CREB/BDNF; miR-221
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