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Blood, Vol. 95 No. 12 (June 15), 2000:
pp. 3951-3958
Estradiol-stimulated nitric oxide release in human granulocytes is
dependent on intracellular calcium transients: evidence of a cell
surface estrogen receptor
George B. Stefano,
Patrick Cadet,
Christophe Breton,
Yannick Goumon,
Vincent Prevot,
Jean
Paul Dessaint,
Jean-Claude Beauvillain,
Ann S. Roumier,
Ingeborg Welters, and
Michel Salzet
From the Neuroscience Research Institute, State
University of New York at Old Westbury, Old Westbury, NY; the Mind/Body
Medical Institute, Beth Israel Deaconess Medical Center, Boston, MA;
Laboratoire d'Endocrinologie des Annélides, Université des
Sciences et Technologies de Lille, Villeneuve d'Ascq Cédex,
France; and INSERM 422, Unité de Neuroendocrinologie et
Physiopathologie Neuronale, and Laboratoire d'Immunologie, Lille
Cedex, France.
We tested the hypothesis that estrogen acutely stimulates
constitutive nitric oxide synthase activity in human granulocytes by
acting on a cell surface estrogen receptor (ER). The release of nitric
oxide was measured in real time with an amperometric probe. Exposure of
granulocytes to 17 -estradiol stimulated NO release within seconds in
a concentration-dependent manner. The NO release was also stimulated by
17-estradiol conjugated to bovine serum albumin
(E2-BSA), which suggests mediation by a cell surface
receptor. Tamoxifen, an ER inhibitor, antagonized the action of both
17-estradiol and E2-BSA, whereas ICI 182,780, an
inhibitor of the nuclear ER, had no effect. Using dual emission microfluorometry in a calcium-free medium, the
17-estradiol-stimulated release of NO from granulocytes was shown
to be dependent on intracellular calcium
([Ca2+]i) transients in a
tamoxifen-sensitive process. Exposure to BAPTA-AM (1,2bis-(-aminophenoxy)ethans-N,N,N',N'-tetraacetic acid
tetra(acetoxyymethyl) ester), a [Ca2+]i chelator,
reduced [Ca2+]i in response to E2-BSA, and
depleting [Ca2+]i stores abolished the effect of
17-estradiol on NO release. Confocal photomicrographs using
E2-BSA-FITC (fluorescein isothiocyanate) revealed cell
membrane reactivity. Estrogen-stimulated NO release had an
immunosuppressive effect, and it initiated granulocyte rounding and
loss of adherence in a tamoxifen-sensitive manner. Finally, using
reverse transcriptase-polymerase chain reaction, human neutrophil
granulocytes expressed ER but not ER, suggesting that ER may
be the membrane receptor for 17-estradiol. The study demonstrated
that a physiological dose of estrogen down-regulates granulocyte
activity by acutely stimulating NO release via the activation of a cell
surface ER which is coupled to increases in [Ca2+]i.
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