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.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Shan T,Zhang L,Zhao C,Chen W,Zhang Y,Li Gdoi
10.3892/mmr.2014.2128subject
Has Abstractpub_date
2014-06-01 00:00:00pages
2180-6issue
6eissn
1791-2997issn
1791-3004journal_volume
9pub_type
杂志文章abstract::More than 60 years after their isolation and characterization, aminoglycoside (AG) antibiotics remain powerful agents in the treatment of severe gram-negative, enterococcal or mycobacterial infections. However, the clinical use of AGs is hampered by nephrotoxicity and ototoxicity, which often develop as a consequence ...
journal_title:Molecular medicine reports
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doi:10.3892/mmr.2017.7631
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2017.7812
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doi:10.3892/mmr.2018.8590
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journal_title:Molecular medicine reports
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doi:10.3892/mmr.2013.1498
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journal_title:Molecular medicine reports
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journal_title:Molecular medicine reports
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doi:10.3892/mmr.2017.6101
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pub_type: 杂志文章
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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