Related Experiment Video
Updated: Aug 13, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
Short synthetic endostatin peptides inhibit endothelial migration in vitro and endometriosis in a mouse model
Christian M Becker1, David A Sampson, Sarah M Short
1Department of Surgery, Vascular Biology Program, Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Objective:
To determine the active peptide regions inside the angiogenesis inhibitor endostatin that can inhibit endothelial migration in vitro and also inhibit endometriosis in a mouse model.
Design:
Pharmacologic intervention in a surgically induced mouse model of endometriosis and endothelial migration assay.
Setting:
Animal research and laboratory facility.
Subject(S):
Eight-week-old, female C57BL/6 mice and human microvascular endothelial cells.
Intervention(S):
Eight overlapping synthetic peptides were tested for inhibitory potential on endothelial migration in vitro. The peptides with significant activity then were given for 4 weeks to mice after implantation of autologous endometrium.
Main Outcome Measure(S):
Inhibition of vascular endothelial growth factor-induced endothelial migration for in vitro studies. In vivo studies examined the growth rate of endometriotic lesions after 4 weeks of treatment, as well as the effect on estrous cycling and ovulation as assessed by corpus luteum formation.
Result(S):
The N-terminal mP-1 peptide and the internal mP-6 peptide inhibited endothelial migration in a dose-dependent manner. Additionally, both synthetic peptides suppressed growth of endometriotic lesions significantly in vivo. However, estrous cycling and corpus luteum formation were normal in both groups.
Conclusion(S):
Short endostatin fragments may be promising as a new, nontoxic therapeutic strategy for the treatment of endometriosis without inhibition of normal estrous cycles.
