Elevated p-selectin on platelets in depression: response to bupropion

increased platelet activation has been suggested as a possible reason for the increased vulnerability of depressed patients to ischemic heart disease (IHD). Translocation of p-selectin, an integral alpha -granule membrane protein, to the platelet surface is a measure of platelet activation. Herein, western blots of platelet plasma membranes containing p-selectin were quantified in patients with major depression (it = 19: mean age = 39 +/- 2 years) and healthy comparison subjects (n = 17; mean age = 36 +/- 2 years). None evidenced clinical signs of IHD, and only two patients had a lifestyle IHD risk factor (smoking), Blood was obtained from all 19 depressed patients before treatment, and 15 returned after 6-8 weeks of open-label bupropion treatment. Bupropion was chosen as the antidepressant because it did not elevate plasma norepinephrine or serotonin, endogenous agonists that can induce platelet degranulation. Western blotting revealed more p-selectin immunoreactivity (75 kD band) in depressed patients compared to healthy controls (P = 0.003). After bupropion treatment, p-selectin remained high in depressed patients. beta3-Integrin; a reference plasma membrane protein that does not translocate during activation, was of equivalent density in depressed patients and healthy control subjects, and was unchanged after treatment with bupropion. p-Selectin failed to correlate with severity of illness based on the Hamilton Depression scale, or with the post-treatment plasma concentration of bupropion. The results suggest an elevation in p-selectin on platelet plasma membranes might be a trait marker for depression. (C) 2001 Elsevier Science Ltd. All rights reserved.