Notch1 signaling enhances collagen expression and fibrosis in mouse uterus

In this study, we further detected expressions of all 44 collagen genes in these Notch1 gain-of-function transgenic mice and found that 18 collagens have been largely affected. In another aspect, using an intrauterine adhesion model (IUA), we mimicked fibrosis in the mouse uterine. The results suggested that Notch receptors were upregulated only 3  days after induction, and most of the fibril-forming collagen began to upregulate 6 days after the surgery. Furthermore, when induced IUA in the N1ICD-OEx mice, the expression of collagens and fibrosis levels were significantly enhanced. At last, as a Notch signaling inhibitor, the γ-secretase inhibitor N-[N-(3,5-difl uorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) pretreatment could alleviate the expression of collagens and the symptoms of fibrosis. These results demonstrate that Notch signaling may play a role in upregulating collagens expression in endometrial fibrosis and might be a potential target of fibrosis therapy in the endometrium.

Source: BioFactors - July 29, 2021 Category: Biochemistry Authors: Qi ‐Xin Xu, Wang‐Qing Zhang, Xiao‐Zheng Liu, Wan‐Kun Yan, Lei Lu, Shan‐Shan Song, Shu‐Wen Wei, Ying‐Nan Liu, Jin‐Wen Kang, Ren‐Wei Su Tags: Research Communication Source Type: research