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Endothelial-monocyte-activating polypeptide II

M P Tas1, J C Murray

  • 1CRC Department of Clinical Oncology, University of Nottingham, City Hospital, U.K.

The International Journal of Biochemistry & Cell Biology
|August 1, 1996
PubMed
Summary
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Endothelial-monocyte-activating polypeptide II (EMAP II) is a protein that causes inflammation and tumor regression. EMAP II may also induce programmed cell death, acting as an anti-angiogenic factor.

Area of Science:

  • Biochemistry
  • Immunology
  • Cell Biology

Background:

  • Endothelial-monocyte-activating polypeptide II (EMAP II) is derived from fibrosarcoma cells.
  • It is synthesized as a precursor (proEMAP) and cleaved into an active 22 kDa form.
  • EMAP II influences endothelial cells, monocytes, and neutrophils.

Purpose of the Study:

  • To investigate the dual role of EMAP II.
  • To determine if EMAP II is primarily pro-inflammatory or an inducer of apoptosis.

Main Methods:

  • Isolation and characterization of mature EMAP II.
  • In vitro modulation of endothelial cells, monocytes, and neutrophils.
  • In vivo studies of inflammatory reactions and tumor regression.
  • Assessment of EMAP II's role in endothelial cell apoptosis.

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Main Results:

  • EMAP II modulates endothelial cells, monocytes, and neutrophils in vitro.
  • EMAP II induces acute inflammation and tumor regression in vivo.
  • Evidence suggests EMAP II induces endothelial cell apoptosis, indicating an anti-angiogenic function.

Conclusions:

  • EMAP II exhibits pro-inflammatory and anti-tumorigenic properties.
  • EMAP II's ability to induce apoptosis suggests a novel role in programmed cell death.
  • Further research is needed to clarify EMAP II's primary function as a cytokine or mediator of apoptosis.