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Related Concept Videos

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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17 beta-estradiol increases inducible nitric oxide synthase expression in macrophages.

Ho Jin You1, Ji Young Kim, Hye Gwang Jeong

  • 1Department of Pharmacy and Research Center for Proteineous Materials, Chosun University, 375 Seosuk-dong, Kwangju 501-759, Republic of Korea.

Biochemical and Biophysical Research Communications
|April 10, 2003
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17beta-estradiol (E2) increases nitric oxide (NO) production in rat macrophages by upregulating inducible nitric oxide synthase (iNOS) expression. This effect is mediated through estrogen receptors (ERs), demonstrating a receptor-mediated pathway.

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Area of Science:

  • Immunology
  • Endocrinology
  • Molecular Biology

Background:

  • 17beta-estradiol (E2) is known to modulate endothelial nitric oxide synthase (eNOS) in certain tissues.
  • Estrogen receptors (ERalpha and ERbeta) play crucial roles in mediating the effects of E2.
  • Nitric oxide synthase (NOS) exists in different isoforms, including inducible NOS (iNOS), which is involved in inflammatory responses.

Purpose of the Study:

  • To investigate the effects of E2 on ERalpha, ERbeta, and iNOS expression in rat peritoneal macrophages.
  • To elucidate the underlying mechanisms of E2-induced NO production in these cells.
  • To determine if E2 stimulates iNOS expression via a receptor-mediated pathway.

Main Methods:

  • Reverse-transcription polymerase chain reaction (RT-PCR) to quantify mRNA levels of ERalpha, ERbeta, and iNOS.
  • Transient transfection assays using a luciferase reporter plasmid under the control of estrogen-responsive elements.
  • Incubation of rat peritoneal macrophages with varying concentrations of E2.
  • Coincubation with ICI 182.780, an estrogen receptor antagonist.

Main Results:

  • Rat peritoneal macrophages express both ERalpha and ERbeta mRNA and are responsive to E2.
  • E2 treatment led to increased ERbeta mRNA expression.
  • E2 induced a dose-dependent increase in NO production, with significant effects at concentrations above 10(-11)M.
  • Increased NO production correlated with elevated iNOS mRNA levels, as shown by RT-PCR.
  • The estrogen receptor antagonist ICI 182.780 inhibited E2-induced NO production and iNOS expression.

Conclusions:

  • E2 stimulates iNOS expression in rat peritoneal macrophages.
  • This stimulation occurs through a classic estrogen receptor-mediated pathway.
  • E2's effect on iNOS expression is a consequence of ER activation.