Abstract
Intrauterine adhesions (IUA) may be caused by endometrial stromal cell proliferation, increases in myofibroblasts or increases in extracellular matrix secretion. However, the specific mechanisms underlying the development of IUA have yet to be elucidated. The present study identified that angiotensin (Ang) II is capable of promoting endometrial epithelium cell (EEC) proliferation and the transdifferentiation of EECs into myofibroblasts. Furthermore, the present study found that Ang II increased the expression of the myofibroblast specific protein α-smooth muscle actin (α-SMA), decreased the expression and secretion of E-cadherin, and increased the synthesis of collagen type I (Col I) and fibronectin (FN). However, Ang-(1-7) was observed to inhibit Ang II-induced proliferation and transdifferentiation of EECs, decrease the expression of α-SMA, increase the expression of E-cadherin and decrease the synthesis and secretion of Col Ⅰ and FN. These findings suggest that Ang-(1-7) is capable of inhibiting the Ang II-induced proliferation and transdifferentiation of human EECs and decreases in Col I and FN secretion. The present study may provide insight into the mechanism underlying endometrial fibrosis.