The correlation between adiponectin and FGF9 in depression disorder
Xiao-Qing Wang1, Wei-Hui Li2, Ya-Hui Tang3
1XiangYa Pharmacy School, Central South University, Changsha 410083, China; Hunan Center for Safety Evaluation and Research of Drugs & Hunan Key Laboratory for Pharmacodynamics and Safety Evaluation of New Drugs, Changsha 410013, China.
Brain Research
|December 15, 2019
Summary
Adiponectin (ADPN) and fibroblast growth factor 9 (FGF9) levels are altered in depression. This study reveals ADPN negatively regulates FGF9, suggesting a key role in stress-induced depression.
Area of Science:
- Neuroscience
- Endocrinology
- Molecular Biology
Background:
- Adiponectin (ADPN) acts as an anti-depressive factor, while fibroblast growth factor 9 (FGF9) is pro-depressive.
- The direct interaction between ADPN and FGF9 in the context of depression remains unexplored.
Purpose of the Study:
- To investigate the correlation between ADPN and FGF9 in individuals with depression disorder.
- To elucidate the role of the ADPN-FGF9 pathway in stress-induced depression.
Main Methods:
- Plasma ADPN and FGF9 levels were measured in depressive patients and non-depressive subjects.
- Depressive-like behaviors and hippocampus changes were assessed in adiponectin knockout mice and chronic unpredictable mild stress (CUMS)-induced depression mouse models.
- Recombinant ADPN, FGF9 antibody, and anti-FGF9 treatments were administered in vivo.
Main Results:
- Depressive patients exhibited decreased ADPN and increased FGF9 levels, with a negative correlation between the ADPN/FGF9 ratio and depression scores.
- CUMS-induced depression in mice showed similar alterations in ADPN and FGF9, accompanied by hippocampus damage, which were ameliorated by ADPN or FGF9 antibody treatment.
- FGF receptor 3 (FGFR3) expression was downregulated in CUMS mice and restored by ADPN or anti-FGF9 treatment.
Conclusions:
- ADPN functions as a negative regulator of the FGF9/FGFR3 pathway in depressive disorder.
- Dysfunction of the ADPN-FGF9 pathway is implicated in the pathophysiology of stress-induced depression.
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