Philippine Journal of Science
152 (3): 1039–1052, June 2023
ISSN 0031 – 7683
Date Received: 27 Sep 2022

Non-surgical Syngeneic Model of Endometriosis
in Ovary-intact Outbred Mice

Irene L. Tan1,2, Kimberly B. Benjamin3, Prince Dominik Alljen C. Tan1,
Emmanuel Marc C. Reyes1, Joseph S. Masangkay4, and Michael C. Velarde1*

1Institute of Biology, College of Science,
University of the Philippines Diliman, Quezon City 1101 Philippines
2Division of Natural Sciences and Mathematics, University of the Philippines
Visayas Tacloban College, Tacloban City, Leyte 6500 Philippines
3Department of Biology, College of Arts and Sciences, University of the Philippines
Manila, Padre Faura St., Taft Ave, Ermita Manila 1100 Philippines
4Department of Veterinary Paraclinical Sciences, College of Veterinary Medicine,
University of the Philippines Los Baños 4030 Philippines

*Corresponding author: mcvelarde@up.edu.ph

[Download]
Tan I et al. 2023. Non-surgical Syngeneic Model of Endometriosis in Ovary-intact
Outbred Mice. Philipp J Sci 152(3): 1039–1052. https://doi.org/10.56899/152.03.24

 

ABSTRACT

Intraperitoneal injection of endometrial tissues into inbred mice such as C57BL/6J is widely used as a model to study endometriosis, a disease characterized by the abnormal proliferation of endometrial cells which invade various tissues within the peritoneal cavity. However, most of these inbred mouse strains have a weak immune system and are often ovariectomized, which is not reflective of the human population in general. Hence, this study used the ovary intact ICR mouse strain as a model to study the immune response during endometriosis development using a non-surgical syngeneic model with no estrogen supplementation. We showed that ICR mice developed ectopic endometrial tissues after 8 wk, but these were mostly necrotic. Reducing the induction period to 4 wk increased the number of ectopic tissues, and endometriotic lesions were also formed in 30% of the induced recipient mice, albeit with a relatively low incidence rate. Endometriotic lesions in ICR mice were also associated with fewer lesion-resident macrophages and lesser vascularization than in C57BL/6J mice. This is further supported by a significantly downregulated expression of genes involved in angiogenesis and M2 macrophage activity in ICR versus C57BL/6J donor endometrium. Conversely, inflammatory response genes were significantly upregulated in the endometrium of ICR versus C57BL/6J mice. Overall, these data implicate the role of inflammation in inhibiting the establishment of endometrial lesions in ICR mice and the involvement of macrophage in promoting endometriosis in C57BL/6J mice. The present work reports the establishment of endometriotic lesions in outbred ICR mice by a less invasive syngeneic intraperitoneal injection procedure.