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Growth Hormone Increases Vascular Cell Adhesion Molecule 1 Expression: in Vivo and in Vitro Evidence

Immunoendocrine Research Unit (T.K.H.), Medical Department M (Endocrinology and Diabetes) (T.K.H., S.F., R.D., J.O.L.J.), and Research Laboratory for Biochemical Pathology, Institute of Pathology (T.L., L.M.R.), University Hospital of Aarhus, Kommunehospitalet, DK-8000 Aarhus C, Denmark

Address all correspondence and requests for reprints to: Troels Krarup Hansen, M.D., Ph.D., Medical Department M (Endocrinology and Diabetes), Aarhus University Hospital, Norrebrogade 42-44, DK-8000 Aarhus C, Denmark. E-mail: tkh{at}dadlnet.dk.

We investigated the impact of GH administration on endothelial adhesion molecules, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin, in vivo and in vitro. Soluble VCAM-1, E-selectin, and C-reactive protein concentrations were measured before and after treatment in 25 healthy subjects and 25 adult GH-deficient (GHD) patients randomized to GH treatment or placebo. Furthermore, we studied the direct effect of GH and IGF-I and serum from GH-treated subjects on basal and TNF-stimulated expression of VCAM-1 and E-selectin on cultured human umbilical vein endothelial cells. Baseline levels of VCAM-1, but not E-selectin, were significantly lower in GHD patients than in healthy subjects (362 ± 15 µg/liter vs. 516 ± 21 µg/liter, P < 0.001) and increased in GHD patients during GH treatment, compared with placebo [net difference between groups 151.8 µg/liter (95% confidence interval: 95.0–208.7 µg/liter); P < 0.0001]. In human umbilical vein endothelial cells, there was no direct stimulatory effect of either GH or IGF-I on the expression of VCAM-1 and E-selectin, but serum from GH-treated healthy subjects significantly increased the expression of VCAM-1 (P < 0.01). Our findings are compatible with the notion that GH may stimulate the expression of VCAM-1 indirectly through modulation of circulating factors. VCAM-1-mediated leukocyte extravasation is implicated in several illnesses including atherosclerosis and multiple-organ failure in sepsis, and we hypothesize that enhanced expression of VCAM-1 may contribute to the detrimental effects of GH in critically ill patients.

This work was supported by grants from the Danish Research Council (Novo Nordisk Center for Research in Growth and Regeneration, Aarhus University, Grant 960082) and the Danish Heart Foundation.

Abbreviations: CRP, C-reactive protein; GHD, GH-deficient; HRP, horseradish-peroxidase; HUVEC, human umbilical vein endothelial cell;MOF, multiple-organ failure; VCAM-1, vascular cell adhesion molecule-1.

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