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Prolactin induces MFG-E8 production in macrophages via transcription factor C/EBPbeta-dependent pathway

Md Monowar Aziz1, Shunji Ishihara, Mohammad Azharul Karim Rumi

  • 1Department of Internal Medicine II, Shimane University School of Medicine, 89-1, Enya-cho, Izumo, Shimane, Japan.

Apoptosis : an International Journal on Programmed Cell Death
|April 9, 2008
PubMed

Insights

Prolactin (PRL) significantly increases milk fat globule epidermal growth factor 8 (MFG-E8) expression in macrophages, enhancing their ability to clear apoptotic cells. This effect is mediated by the C/EBPbeta binding site within the MFG-E8 promoter.

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Prolactin (PRL) is a lactogenic hormone crucial for mammary gland function.
  • Milk fat globule epidermal growth factor 8 (MFG-E8) is essential for the clearance of apoptotic cells, maintaining bodily homeostasis.
  • The regulatory mechanisms of MFG-E8 expression, particularly in response to PRL, are not fully understood.

Purpose of the Study:

  • To investigate the effect of prolactin (PRL) on milk fat globule epidermal growth factor 8 (MFG-E8) expression in macrophages.
  • To elucidate the promoter mechanisms underlying PRL-induced MFG-E8 expression.
  • To assess the functional consequence of PRL on macrophage phagocytosis.

Main Methods:

  • Macrophages were treated with PRL and MFG-E8 expression was quantified using real-time PCR and Western blotting.
  • Luciferase reporter assays were employed to evaluate MFG-E8 promoter activity.
  • Electrophoretic mobility shift assays (EMSA) were used to assess C/EBPbeta binding activity.

Main Results:

  • PRL treatment led to significant upregulation of the PRL receptor and MFG-E8 expression in macrophages.
  • Macrophage phagocytosis of apoptotic cells was enhanced following PRL stimulation.
  • MFG-E8 promoter analysis revealed PRL-induced activation, primarily mediated by the C/EBPbeta binding site, which showed increased activity.

Conclusions:

  • Prolactin (PRL) is a potent inducer of MFG-E8 expression in macrophages.
  • PRL enhances macrophage phagocytic capacity through the upregulation of MFG-E8.
  • The PRL-mediated induction of MFG-E8 expression involves activation of the C/EBPbeta binding site in its promoter.

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