Previous findings show lack of proven biomarkers for predicting antidepressant drug response. Recent genome-wide expression study indicates CHL-1 gene as potential depression treatment biomarker. Aim of study is to examine possibility of applying CHL-1 gene with a group of Polish depressive patients as SSRI response biomarker. Peripheral blood samples were collected from well clinically characterized naïve (N), treatment resistant (TR) depressive patients and healthy (H) volunteers. Lymphocytes were isolated and cultured with two selected drugs – paroxetine and mirtazapine. Cell proliferation assay was done after 72 h of incubation. The total RNAs from lymphocytes without drugs were extracted and cDNAs were synthetized. Levels of CHL-1 gene expression were checked by real-time PCR method. There are significant differences between chosen phenotypes: high and low sensitivity to mirtazapine for H, TR and N; high and low sensitivity to paroxetine for H and N. There are significant differences between mirtazapine sensitivity for whole groups of H and TR. There are not significant differences of CHL-1 gene expression levels between groups. Findings indicate different phenotypes occurrence for SSRI mediated growth inhibition sensitivity. Conclusions about CHL-1 gene as a SSRI response biomarker are still unclear. Suported by Era-Net-Neuron “PADRE” grant.
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