Abstract
Comparative proteomic analysis of plasma from bipolar depression and depressive disorder: identification of proteins associated with immune regulatory.
Highlights
Immune dysregulation in bipolar II depressionThe complement and coagulation cascade pathways were enriched (P < 0.01) and five proteins were found to be involved in the pathway: C3, CFI, C4BPα,kininogen-1, and antithrombin
Bipolar disorder (BD) is a debilitating psychiatric mood disorder affecting approximately 1%–3% of the population worldwide (Merikangas, 2007)
A proteomic analysis based on two-dimensional electrophoresis (2-DE) coupled with matrix-assisted laser desorption/ionization-time-of-flight/time-of-flight tandem mass spectrometry (MALDI-TOF/TOF MS) was carried out on plasma samples from drug-naïve bipolar II and major depressive disorder (MDD) patients, In order to overcome the limitations of a narrow linear range and large variations in 2-DE, 15 samples were mixed within each study group, and for each group, 2-DE was repeated in triplicate to limit run-to-run variations to about 20%, the criterion of 2-fold change was used as a cut off to ensure the reliability of apparent differences
Summary
The complement and coagulation cascade pathways were enriched (P < 0.01) and five proteins were found to be involved in the pathway: C3, CFI, C4BPα,kininogen-1, and antithrombin. C3, CFI, and C4BPα were included in the pathway of complement cascades (P < 0.05). The quantitative results trends in expression patters were consistent with the MALDI -TOF/TOF MS findings, the changes were smaller than those determined by 2-DE, the differences were statistically significant, and the expression levels of these three proteins being significantly dysregulated with the following profiles: C3, MDD > bipolar II > HC subjects; CFI and C4BPα, HC > MDD > bipolar II subjects (Fig. 2A–C). The findings reported here provide evidence demonstrating that autoimmune dysregulation is involved in the pathophysiological mechanisms either bipolar II or MDD. C3 was considered as a significant feature of complement pathway activation because of its key role in all
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