Circulating Human Heat Shock Protein 60 in the Plasma of British Civil Servants

Abstract

Background-TheWhitehall cohort studies (I and II) of British civil servants have identified sociodemographic, psychosocial, and biological risk factors for coronary heart disease (CHD). To identify mechanisms responsible for susceptibility to CHD, specific biological markers of stress are increasingly being measured. One marker linked to susceptibility to CHD is heat shock protein (Hsp) 60. Methods and Results-Blood was taken from 229 civil servants (126 men and 103 women) in the Whitehall II cohort drawn equally from the range of employment grades. Plasma was assayed for levels of Hsp60, tumor necrosis factor ␣ (TNF␣), C-reactive protein, von Willebrand factor, high density lipoprotein (HDL), total cholesterol, and total/HDL ratio. Psychosocial measures included socioeconomic status, psychological distress, and social isolation. The majority of the participants had Hsp60 in their plasma, and Ϸ20% had Ͼ1000 ng/mL of this protein (a concentration likely to induce biological effects). A positive association between plasma Hsp60 and TNF␣ and a negative association with von Willebrand factor was found. There was also a significant association between elevated Hsp60 levels, low socioeconomic status, and social isolation, together with an association with psychological distress in women. Conclusions-The majority of participants exhibited Hsp60 in their plasma, and there was evidence of an association between levels of this stress protein and the proinflammatory cytokine, TNF␣, and with various psychosocial measures.

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“…In these instances, stressors such as surgical operations [25], intense physical exercises [15,28,85], and short-run psychological stress [16,31] were shown to induce extracellular Hsp70. An extracellular elevation of another kind of chaperon (Hsp60) was also shown to be induced by long-term psychosocial stress [46]. In our previous study, the significant prompt (i.e.…”

Effect of psychological stress on blood pressure increase: a meta-analysis of cohort studies

“…More specifically, heightened cardiovascular reactivity could reflect sympathetic hyperresponsivity or enhanced vagal withdrawal during stress, whereas poorer cardiovascular recovery could be due to prolonged sympathetic activation, diminished vagal tone, or attenuated or delayed vagal rebound following the termination of stress 33 . In addition, several studies have reported associations between psychosocial variables and vascular function 34,35 , inflammation 36 , increased blood clotting and decreased fibrinolysis 37,38 . Reasons for exclusion n = 150 excluded articles n = 100 excluded articles n = 90 quasi-experiments (7 *) n = 22 reviews (5 *) n = 22 crossectional (3 *) n = 7 case-controls (1 *) n = 2 ecological (1 *) n = 2 comments n = 2 clinical trials n = 1 book n = 1 case study n = 1 test-retest Exposure n = 36 occupational (7 *) n = 7 pos-traumatic (2 *) n = 6 stability (2 *) n = 3 hospital internment (2 *) n = 3 risk groups n = 2 financial situation (1 *) n = 2 meditation n = 1 corporal mass n = 1 lifestyle Random effect model, odds ratio for increased blood pressure ≥ 3.5mmHg/hipertension of the effect of responses to stressor tasks in 23 comparison groups from 6 prospective cohorts.…”

Unfolding the relationship between secreted molecular chaperones and macrophage activation states

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