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Endothelial-monocyte-activating polypeptide II
1CRC Department of Clinical Oncology, University of Nottingham, City Hospital, U.K.
Abstract:
Endothelial-monocyte-activating polypeptide II (EMAP II) was initially identified as a product of murine methylcholanthrene A-induced fibrosarcoma cells. The deduced mRNA sequence indicates that EMAP II is synthesised as a 34 kDa precursor molecule (proEMAP) and enzymatically cleaved to produce a biologically active 22 kDa mature polypeptide, which has been isolated and characterised. It modulates a range of properties of endothelial cells, monocytes, and neutrophils in vitro, and induces an acute inflammatory reaction and tumour regression in vivo. Recent evidence suggests that EMAP II can induce apoptosis in endothelial cells, and as such may act in an anti-angiogenic role. The question arises whether EMAP II is primarily a pro-inflammatory cytokine or a novel mediator of programmed cell death.
Insights
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.
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.