Angiotensin-(1-7) and angiotensin Ⅱ induce the transdifferentiation of human endometrial epithelial cells in vitro

Shan,Tieying; Zhang,Lei; Zhao,Chunfang; Chen,Wei; Zhang,Yanan; Li,Guiying

doi:10.3892/mmr.2014.2128

Angiotensin-(1-7) and angiotensin Ⅱ induce the transdifferentiation of human endometrial epithelial cells in vitro

Authors:
- Tieying Shan
- Lei Zhang
- Chunfang Zhao
- Wei Chen
- Yanan Zhang
- Guiying Li
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Affiliations: Department of Histology and Embryology, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China, Department of Histology and Embryology, Hebei Engineering University, Handan, Hebei 056002, P.R. China
Published online on: April 9, 2014 https://doi.org/10.3892/mmr.2014.2128
Pages: 2180-2186
Copyright: © Shan et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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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.

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