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. 2008 Dec;295(6):E1495-501.
doi: 10.1152/ajpendo.90718.2008. Epub 2008 Oct 21.

Oxytocin attenuates NADPH-dependent superoxide activity and IL-6 secretion in macrophages and vascular cells

Angela Szeto  1 , Daniel A Nation, Armando J Mendez, Juan Dominguez-Bendala, Larry G Brooks, Neil Schneiderman, Philip M McCabe
Affiliations

Oxytocin attenuates NADPH-dependent superoxide activity and IL-6 secretion in macrophages and vascular cells

Angela Szeto et al. Am J Physiol Endocrinol Metab. 2008 Dec.

Abstract

Oxytocin is synthesized and released in the heart and vasculature, tissues that also express oxytocin receptors. Although it has been established this intrinsic cardiovascular oxytocin system is important in normal homeostatic cardiac and vascular regulation, a role for this system in cardiovascular pathophysiology has not been investigated. The current study examined the influence of oxytocin on mechanisms in atherogenesis, oxidative stress, and inflammation in cultured human vascular cells, THP-1 monocytes, and macrophages. Oxytocin receptor protein and mRNA expression, NADPH-dependent superoxide activity, and interleukin-6 secretion were measured. Results demonstrated oxytocin receptor protein and mRNA in THP-1 monocytes and macrophages. Incubation of cells at physiological levels of oxytocin significantly decreased basal and stimulated NADPH-dependent superoxide activity in vascular cells, monocytes, and macrophages by 24-48%. Oxytocin also attenuated interleukin-6 secretion from stimulated THP-1 macrophages and endothelial cells by 56 and 26%, respectively. These findings suggest that oxytocin attenuates vascular oxidative stress and inflammation, two important pathophysiological processes in atherosclerosis. The fact that oxytocin receptors are found in monocytes and macrophages, and oxytocin decreases both superoxide production and release of a proinflammatory cytokine from these cells, suggests a potentially larger role for oxytocin in the attenuation of disease.

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Figures

Fig. 1.
Fig. 1.
Oxytocin receptor mRNA expression in aortic endothelial and smooth muscle cells and THP-1 monocytes and macrophages were quantified using real-time PCR normalized to expression of endothelial cells. Data are means ± SE and from 3 independent experiments.
Fig. 2.
Fig. 2.
A: expression of oxytocin receptor protein expression in human aortic endothelial cells (HAEC), smooth muscle cells, and THP-1 monocytes and macrophages. B: oxytocin receptor protein expression in THP-1 macrophages after differential centrifugation. C: oxytocin receptor protein expression in THP-1 macrophages treated with PNGase-F.
Fig. 3.
Fig. 3.
Effect of oxytocin on NADPH-dependent superoxide production in THP-1 monocytes (A) and macrophages (B), endothelial cells (C), and smooth muscle cells (D). NADPH oxidase activity from cells was detected by lucigenin chemiluminescence. Data are means ± SE and from 3 independent experiments. *P < 0.05 vs. control.
Fig. 4.
Fig. 4.
Effect of oxytocin on total NADPH-dependent superoxide production in TNF-stimulated endothelial cells. Data are means ± SE and from 3 independent experiments. *P < 0.05 vs. TNF-stimulated cells.
Fig. 5.
Fig. 5.
Effect of oxytocin on IL-6 secretion from LPS-stimulated cells. THP-1 macrophages (A) and endothelial cells (B) treated with LPS (100 ng/ml) were incubated with 10 or 100 pM oxytocin, and IL-6 secretion was measured after 6 h. Data are means ± SE and from 3 independent experiments. *P < 0.01, **P < 0.001 vs. LPS-stimulated cells.
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