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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e141.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Circulating Human Heat Shock Protein 60 in the Blood of Healthy Teenagers: A Novel Determinant of Endothelial Dysfunction and Early Vascular Injury?

Julian P.J. Halcox; John Deanfield

Vascular Physiology Unit, Department of Cardiology, Institute of Child Health, University College London

Alireza Shamaei-Tousi; Brian Henderson

Division of Microbial Diseases, Eastman Dental Institute, University College London

Andrew Steptoe

Department of Epidemiology and Public Health, University College London

Anthony R.M. Coates

Department of Cellular and Molecular Medicine, St George’s Hospital Medical School, London

Atul Singhal; Alan Lucas

MRC Childhood Nutrition Research Centre Institute of Child Health, University College London, UK

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Damage and dysfunction of vascular endothelial cells plays a critical role in the initiation and progression of atherosclerosis, with inflammation implicated as a key mediator of endothelial dysfunction and early structural arterial disease in childhood.¹ However, the specific molecular triggers of local vascular inflammation are less clear. One potential mediator relevant to endothelial dysfunction and atherogenesis is heat-shock protein 60 (HSP60).²

HSP60 may act as an intercellular signaling molecule that can activate a variety of cells and has been identified in human atheroma.^3,4 Intracellular soluble HSP60 (sHSP60) has also been identified in the blood of healthy adults,^5,6 sHSP60 levels correlate with measures of psychosocial stress⁵ and are elevated in early carotid disease implicating HSP60 in atherogenesis.⁷

To explore a potential role for HSP60 in early atherogenesis we determined whether sHSP60 was detectable in the blood of healthy adolescents and examined the relationship with clinical measures of vascular function and structural arterial pathophysiology. Young study populations minimize potentially confounding influences of long-term modest risk factor exposure, increasing the ability to evaluate the clinical impact of novel putative atherogenic determinants.

We studied 294 healthy adolescents (aged 13 to 16 years). All subjects were nonsmokers and free from hypertension, dyslipidemia, and diabetes mellitus. Anthropometric, demographic, and metabolic characteristics of this cohort have been published previously.⁸ All subjects underwent noninvasive assessment of flow-mediated vasodilatation (FMD) and distensibility of the brachial artery using high resolution ultrasound to determine endothelial function and arterial stiffness, respectively.⁸ Serum sHSP60 was assayed using a highly specific . . . [Full Text of this Article]

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