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Steroid hormone receptor expression and function in microglia.

Amanda Sierra1, Andres Gottfried-Blackmore, Teresa A Milner

  • 1Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021, USA.

Glia
|February 21, 2008
PubMed
Summary
This summary is machine-generated.

Adult microglia express steroid hormone receptors, including glucocorticoid receptor (GR) and estrogen receptor alpha (ERalpha). Glucocorticoids, not estrogens, primarily regulate microglial inflammatory activity, with receptor expression decreasing after inflammatory challenges.

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Area of Science:

  • Neuroimmunology
  • Endocrinology
  • Cellular Biology

Background:

  • Steroid hormones (glucocorticoids, estrogens) modulate peripheral immunity and brain inflammation.
  • Microglia are key immune cells in the brain, but their expression of steroid hormone receptors is debated.

Purpose of the Study:

  • To investigate the expression and function of steroid hormone receptors in adult microglia.
  • To determine the role of these receptors in microglial inflammatory responses.

Main Methods:

  • Real-time RT-PCR and Fluorescence-activated cell sorting (FACS) to quantify receptor mRNA in isolated microglia.
  • Immunoelectron microscopy to confirm receptor presence in vivo.
  • In vitro assays to assess the impact of estrogens and glucocorticoids on microglial inflammatory profiles.

Main Results:

  • Microglia express glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and estrogen receptor alpha (ERalpha), with GR being most abundant.
  • GR, MR, and ERalpha expression significantly decreased in microglia following an inflammatory challenge.
  • Corticosterone demonstrated consistent anti-inflammatory effects in vitro, while 17beta-estradiol showed minimal impact.

Conclusions:

  • Adult microglia are direct targets of steroid hormones, with glucocorticoids being primary regulators of microglial inflammatory activity.
  • Down-regulation of steroid hormone receptors post-inflammation may impair endogenous anti-inflammatory signaling, promoting sustained microglial activation.