Morphological Remodeling in Mouse Uteri Caused by Hormone Hypersecretion-Induced Increase in MMP Activity

Hormonal hypersecretion is important for the development and physiological function of ovary and uterus. PMSG, progesterone, and testosterone maintain the ovarian cycle of the uterus and regulate physiological mechanisms. However, how hormone hypersecretion causes uterine remodeling is unknown. we investigated uterine remodeling and MMP function in mice, induced by hormone hypersecretion after estrus synchronization. PMSG, progesterone, and testosterone were injected into six six-week-old mice for 14 d to induce hypersecretion. Evaluation of morphological remodeling of the uterus and expression pattern of MMP2 showed that hormone hypersecretion affected the endometrial cells and caused abnormal changes in the glandular cell zone. Notably, PMSG injection caused uterine hypertrophy. Normal MMP expression was observed; however, the expression of the MMP inhibitor TIMP was low. Progesterone did not affect uterine remodeling significantly and the uterus was unaffected by MMP and TIMP expression. However, testosterone caused morphological remodeling in the entire uterus, especially in the glandular cell zone, which is important for uterine function and physiology, and increased the MMP activity. Thus, hormone hypersecretion induced uterine remodeling by regulating MMP function. Additionally, testosterone caused uterine contractions by increasing the MMP activity, which is important for endometrial remodeling.