Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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Originally published online as doi:10.1189/jlb.0108035 on May 30, 2008

Published online before print May 30, 2008
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(Journal of Leukocyte Biology. 2008;84:397-405.)
© 2008 by Society for Leukocyte Biology

Heme oxygenase-1 expression is down-regulated by angiotensin II and under hypertension in human neutrophils

Gonzalo Alba*, Rajaa El Bekay{dagger}, Pedro Chacón*, M. Edith Reyes*, Eladio Ramos{ddagger}, Josefina Oliván{ddagger}, Juan Jiménez*, José M. López§, José Martín-Nieto, Elízabeth Pintado* and Francisco Sobrino*,1

* Departamento de Bioquímica Médica y Biología Molecular,
{ddagger} Unidad de Riesgo Cardiovascular, Hospital Universitario Virgen Macarena,
§ Unidad de Cirugía Vascular, Hospital Universitario Virgen de Valme, Universidad de Sevilla, Spain;
{dagger} Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto de Salud Carlos III, Madrid, and Fundación Imabis, Malaga, Spain; and
Departamento de Fisiología, Genética y Microbiología, Universidad de Alicante, Spain

1 Correspondence: Dpto. Bioquímica Médica y Biología Molecular, Facultad de Medicina, Avda. Sánchez Pizjuán 4, Universidad de Sevilla, E-41009 Sevilla, Spain. E-mail: fsobrino{at}us.es

ABSTRACT

Angiotensin II (Ang II) is a peptide hormone able to elicit a strong production of reactive oxygen species by human neutrophils. In this work, we have addressed whether expression of heme oxygenase-1 (HO-1), an antioxidant enzyme, becomes altered in these cells upon Ang II treatment or under hypertension conditions. In neutrophils from healthy and hypertensive subjects, induction of HO-1 mRNA and protein expression with a parallel increase in enzyme activity took place upon treatment with 15-deoxy-{Delta}12,14-PGJ2 (15dPGJ2). However, Ang II prevented HO-1 synthesis by normal neutrophils in vitro, and HO-1 expression was depressed in neutrophils from hypertensive patients in comparison with cells from healthy subjects. In addition, Ang II treatment led to a reduced HO-1 enzyme activity to levels similar to those found in neutrophils from hypertensive patients. NO donors reversed the inhibition of 15dPGJ2-dependent HO-1 expression in neutrophils from hypertensive patients, and conversely, inhibition of inducible NO synthase (NOS2) activity counteracted the stimulatory effect of 15dPGJ2 on HO-1 expression in normal human neutrophils. Moreover, Ang II canceled 15dPGJ2-dependent induction of NOS2 mRNA synthesis. Present findings indicate that down-regulation of HO-1 expression in neutrophils from hypertensive subjects is likely exerted through the inhibition of NOS2 expression. Additionally, they underscore the potential usefulness of NO donors as new, therapeutic agents against hypertension.

Key Words: antioxidant enzymes • polymorphonuclear cells • oxidative stress • nitric oxide






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