Experimental cell research · 2025
Estradiol inhibits endometrial injury by promoting the stability of the KLF15 protein and the recovery of mitochondrial function.
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Zhou Jianghong, Xiong Zhenghua, Long Xicui, Yang Lijuan, Jin Wenjiao, Han Xuesong
Аннотация
BACKGROUND: Endometrial injury (EI) is an important factor leading to infertility, which seriously affects women's fertility and reproductive health. Research indicates that estradiol (E2) therapy can promote the repair of EI, but the specific mechanism of E2 action in EI remains unclear.
METHODS: The research involved creating an EI model for human endometrial epithelial cells (hEECs) using lipopolysaccharide (LPS), and constructing a rat intrauterine adhesion (IUA) model through simulating mechanical injury of human endometrial. Western blot, immunohistochemistry and RT-qPCR were used to detect the expression of key proteins and genes; endometrial damage was detected by HE, TUNEL and Masson staining; mitochondrial function changes were detected by detecting ROS, ATP levels and mitochondrial membrane potential.
RESULTS: Our research revealed a reduced expression of E2 and Krüppel-like factor 15 (KLF15) in IUA rats. Exogenous E2 treatment inhibited EI by activating the expression of KLF15, inhibited the expression of apoptosis-related proteins Bax and cleaved caspase-3, and promoted the expression of Bcl-2 protein. Additionally, our findings revealed that treatment with E2 decreased mitochondrial ROS (mROS) levels, enhanced mitochondrial membrane potential, and promoted ATP production in EI model cells, whereas KLF15 interference weakens the therapeutic effect of E2, suggesting that E2 treatment alleviates EI by promoting the expression of KLF15 and restoring mitochondrial function. In addition, E2 promotes PGC-1α expression by inhibiting WWP1-mediated ubiquitination degradation of KLF15, thereby restoring mitochondrial function and easing the development of EI.
CONCLUSION: Our study reveals that E2 alleviates EI progression by stabilizing KLF15 protein and restoring mitochondrial function, providing potential targets for EI treatment.
METHODS: The research involved creating an EI model for human endometrial epithelial cells (hEECs) using lipopolysaccharide (LPS), and constructing a rat intrauterine adhesion (IUA) model through simulating mechanical injury of human endometrial. Western blot, immunohistochemistry and RT-qPCR were used to detect the expression of key proteins and genes; endometrial damage was detected by HE, TUNEL and Masson staining; mitochondrial function changes were detected by detecting ROS, ATP levels and mitochondrial membrane potential.
RESULTS: Our research revealed a reduced expression of E2 and Krüppel-like factor 15 (KLF15) in IUA rats. Exogenous E2 treatment inhibited EI by activating the expression of KLF15, inhibited the expression of apoptosis-related proteins Bax and cleaved caspase-3, and promoted the expression of Bcl-2 protein. Additionally, our findings revealed that treatment with E2 decreased mitochondrial ROS (mROS) levels, enhanced mitochondrial membrane potential, and promoted ATP production in EI model cells, whereas KLF15 interference weakens the therapeutic effect of E2, suggesting that E2 treatment alleviates EI by promoting the expression of KLF15 and restoring mitochondrial function. In addition, E2 promotes PGC-1α expression by inhibiting WWP1-mediated ubiquitination degradation of KLF15, thereby restoring mitochondrial function and easing the development of EI.
CONCLUSION: Our study reveals that E2 alleviates EI progression by stabilizing KLF15 protein and restoring mitochondrial function, providing potential targets for EI treatment.