Publication Date




Embargo Period


Degree Type


Degree Name

Master of Science (MS)


Psychology (Arts and Sciences)

Date of Defense


First Committee Member

Philip M. McCabe

Second Committee Member

Neil Schneiderman

Third Committee Member

Armando J. Mendez

Fourth Committee Member

Angela Szeto


Psychosocial stress is related to cardiovascular disease (CVD) morbidity and mortality, but the mechanisms of this relationship remain incompletely understood. The present in vitro study investigated the effect of catecholamines, a subclass of stress hormones, on the early CVD processes of monocyte adhesion and migration. For adhesion, THP-1 monocytes (MO) and human aortic endothelial cells (HAEC) were separately treated with catecholamines prior to static adhesion assay. MO migration was investigated using a Transwell migration protocol. HAEC adrenergic receptor mRNA expression and HAEC adhesion molecule surface expression were evaluated. Adrenergic agonism/antagonism experiments were utilized to determine the role of specific adrenergic receptor subtypes in adhesion and migration. Catecholamine treatment of HAEC, but not MO, increased adhesion of MO to HAEC, which was attenuated by B2-adrenergic receptor blockade. B-adrenergic activation also increased surface expression of intercellular adhesion molecule-1. Catecholamine treatment did not increase production of pro-inflammatory cytokines known to enhance cellular adhesion, suggesting a direct effect of catecholamines. Catecholamines were also mildly chemotactic for MO. These results provide a mechanism by which psychosocial stress, working through catecholamines, could promote early CVD processes of MO adhesion and migration.


Atherosclerosis; catecholamines; adrenergic receptors; vascular endothelial cells; monocytes; cellular adhesion