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Nongenomic estrogen effects on nitric oxide synthase activity in rat adipocytes

Anne-Marie Jaubert1, Nadia Mehebik-Mojaat, Danièle Lacasa

  • 1Départment de Biochimie et de Biologie Moléculaire, Université de Versailles Saint-Quentine en Yuelines, Versailles, France.

Endocrinology
|February 17, 2007
PubMed

Insights

Estrogens rapidly increase nitric oxide synthase (NOS) activity in fat cells through distinct pathways. These pathways differ based on whether estrogen is free or bound to albumin, highlighting receptor location

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Adipose Tissue Metabolism

Background:

  • Estrogens influence adipose tissue via nuclear receptors and rapid membrane-initiated signaling pathways.
  • Nongenomic estrogen actions involve kinase cascades, impacting cellular metabolism.
  • Nitric oxide (NO) plays a role in adipose tissue function and metabolism.

Purpose of the Study:

  • To investigate the rapid effects of 17-beta estradiol (E2) and its albumin-conjugated form (E2-BSA) on nitric oxide production in white adipose tissue.
  • To elucidate the specific signaling pathways and molecular targets involved in estrogen-mediated nitric oxide synthase (NOS) activation in adipocytes.

Main Methods:

  • Measurement of nitric oxide synthase (NOS) activity in adipocytes treated with E2 and E2-BSA.
  • Pharmacological inhibition of estrogen receptors, phosphatidylinositol 3-kinase (PI3K), protein kinase A (PKA), and MAPK kinase/ERK (p42/p44 MAPKs).
  • Immunoblotting to assess the phosphorylation of endothelial NOS (NOS III) at Ser(1179).

Main Results:

  • Both E2 and E2-BSA stimulated NOS activity in adipocytes.
  • E2-induced NOS activity was dependent on estrogen receptors, PI3K, and PKA.
  • E2-BSA-induced NOS activity was dependent on MAPK kinase/ERK (p42/p44 MAPKs) and also involved estrogen receptors.
  • Both forms of estrogen led to NOS III phosphorylation at Ser(1179), but E2-BSA's effect was specifically blocked by UO126 (MAPK inhibitor).

Conclusions:

  • Estrogen signaling pathways in adipocytes differ based on the estrogen's form (free vs. albumin-conjugated).
  • These findings underscore the importance of estrogen receptor localization in mediating nongenomic effects on adipose tissue.
  • Distinct kinase cascades are activated depending on membrane-initiated versus nuclear estrogen signaling.

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