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Updated: Sep 25, 2026
A Cell Culture Model of Resistance Arteries
Published on: September 8, 2017
Interaction of plasminogen-related protein B with endothelial and smooth muscle cells in vitro
Hideo Morioka1, Takeshi Morii, Tikva Vogel
1Orthopaedic Research Laboratories, Massachusetts General Hospital and Harvard Medical School, GRJ 1124, 55 Fruit Street, Boston, MA 02114, USA.
Abstract:
Plasminogen-related protein B (PRP-B) closely resembles the N-terminal plasminogen activation peptide, which is released from plasminogen during conversion to plasmin. We have previously demonstrated that the steady-state level of mRNA encoding PRP-B is increased within tumor tissues, and that recombinant PRP-B antagonizes neoplastic growth when administered systemically to mice harboring tumors, but no insights into the cell targets of PRP-B have been presented. Employing serum-free medium optimized for culturing human endothelial or smooth muscle cells, we show that recombinant PRP-B inhibits basic fibroblast growth factor-dependent cell migration for both cell types, as well as tube formation of endothelial cells. Comparison with the angiogenesis inhibitors angiostatin and endostatin revealed similar results. Recombinant PRP-B is effective in promoting cell attachment of endothelial and smooth muscle cells, and antibody interference experiments reveal that the interaction of recombinant PRP-B with endothelial cells is mediated at least in part by alpha(v)-containing integrins. Inhibition of angiogenesis in vivo by PRP-B was demonstrated in the chicken chorioallantoic membrane assay. PRP-B and other antiangiogenic molecules may elicit metabolic perturbations in endothelial cells as well as perivascular mesenchymal cells such as smooth muscle cells and pericytes.
Insights
Plasminogen-related protein B (PRP-B) inhibits endothelial and smooth muscle cell functions crucial for tumor growth. This protein demonstrates anti-angiogenic properties, suggesting potential therapeutic applications in cancer treatment.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Plasminogen-related protein B (PRP-B) mRNA levels are elevated in tumor tissues.
- Previous studies showed PRP-B antagonizes tumor growth in mice.
- The cellular targets and mechanisms of PRP-B action remained unclear.
Purpose of the Study:
- To identify the cellular targets of PRP-B.
- To elucidate the mechanisms by which PRP-B affects cell behavior.
- To evaluate the anti-angiogenic potential of PRP-B.
Main Methods:
- Culturing human endothelial and smooth muscle cells in serum-free media.
- Assessing cell migration, tube formation, and cell attachment.
- Utilizing antibody interference assays with alpha(v)-containing integrins.
- Conducting in vivo angiogenesis assays on the chicken chorioallantoic membrane.
Main Results:
- Recombinant PRP-B inhibited basic fibroblast growth factor-dependent migration in both endothelial and smooth muscle cells.
- PRP-B suppressed endothelial cell tube formation.
- PRP-B promoted cell attachment for both cell types.
- PRP-B's interaction with endothelial cells involved alpha(v)-containing integrins.
- PRP-B demonstrated in vivo anti-angiogenic activity.
Conclusions:
- PRP-B exhibits anti-angiogenic properties by inhibiting endothelial cell migration and tube formation.
- PRP-B interacts with endothelial cells via alpha(v)-containing integrins.
- PRP-B may induce metabolic changes in endothelial and perivascular cells, contributing to its anti-tumor effects.
