Role of Prolylcarboxypeptidase in Inflammation
Author Information
Author(s): Ngo My-Linh, Mahdi Fakhri, Kolte Dhaval, Shariat-Madar Zia
Primary Institution: University of Mississippi
Hypothesis
The upregulation of prolylcarboxypeptidase (PRCP) expression in lipopolysaccharide (LPS) treated endothelium promotes inflammation.
Conclusion
Increased PRCP leads to a sustained production of bradykinin in endothelium following LPS treatment, which may contribute to inflammatory vascular disorders.
Supporting Evidence
- PRCP is critical to the maintenance of endothelial cells.
- Significant elevation in kallikrein was seen on LPS-treated HUVECs.
- The conversion of PK to kallikrein was blocked by the inhibitor of PRCP.
- PRCP might be a risk factor for inflammation.
Takeaway
When certain cells in the body are exposed to a bacteria-related substance, they produce more of a protein called PRCP, which can lead to inflammation.
Methodology
The study used RT-PCR to measure PRCP expression and biochemical assays to assess kallikrein activation in LPS-treated human umbilical vein endothelial cells (HUVEC).
Limitations
The study did not specify the exact sample size or the potential variability in cell response to LPS treatment.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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