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Inflammation induces serine protease inhibitor 3 expression in the rat pineal gland

A Takamiya1, M Takeda, A Yoshida

  • 1Department of Anatomy, Asahikawa Medical College, 2-1 Midorigaoka Higashi Asahikawa, Hokkaido 078-8510, Japan.

Neuroscience
|July 20, 2002
PubMed

Insights

Systemic inflammation up-regulates serine protease inhibitor 3 (SPI-3) in rat pinealocytes via STAT3. This suggests SPI-3 may prevent inflammation-induced proteolysis.

Area of Science:

  • Neuroendocrinology
  • Immunology
  • Molecular Biology

Background:

  • Serine protease inhibitor 3 (SPI-3) mRNA expression is prominent in the rat pineal gland following lipopolysaccharide (LPS) administration.
  • SPI-3 mRNA-positive cells in the pineal gland are identified as pinealocytes, not astrocytes.

Purpose of the Study:

  • To investigate the cellular localization and regulatory mechanisms of SPI-3 expression in the rat pineal gland during systemic inflammation.
  • To elucidate the role of signal transducers and activators of transcription 3 (STAT3) and specific cytokine receptors in SPI-3 induction.

Main Methods:

  • Systemic injection of lipopolysaccharide (LPS) in rats.
  • Northern blotting to confirm mRNA expression.
  • Immunohistochemistry to identify cell types and STAT3 nuclear translocation.
  • Analysis of cytokine receptor mRNA expression.

Main Results:

  • LPS treatment significantly up-regulates SPI-3 mRNA in pinealocytes.
  • SPI-3 expression is STAT3-mediated, evidenced by STAT3 nuclear translocation in SPI-3 positive cells.
  • Expression of ciliary neurotrophic factor receptor (CNTFR) and leukemia inhibitory factor receptor (LIFR) mRNAs are also up-regulated by LPS.

Conclusions:

  • Cytokines like LIF and/or CNTF, acting through their receptors and STAT3, likely induce SPI-3 expression in the pineal gland in response to inflammatory stimuli.
  • SPI-3 may play a protective role against proteolysis in the pineal gland during systemic inflammation.

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