Activation of the MAPK/ERK Cell-Signaling Pathway in Uterine Smooth Muscle Cells of Women With Adenomyosis
Uterine smooth muscle cells from women with adenomyosis show increased proliferation and MAPK/ERK pathway activation, independent of ROS, suggesting these pathways' implication in proliferation.
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The paper investigated whether uterine smooth muscle cells (uSMCs) from women with adenomyosis show intrinsic differences in activation of MAPK/ERK and PI3K/mTOR/AKT signaling pathways, and whether reactive oxygen species (ROS) production is involved. uSMCs were cultured from myometrium biopsies collected during hysterectomy or myomectomy from women with adenomyosis and controls with leiomyoma, and the authors assessed pathway activation, uSMC proliferation, and ROS production/detoxification. They found increased uSMC proliferation and increased in vitro MAPK/ERK activation in adenomyosis versus controls, while PI3K/mTOR/AKT activation was not significantly different and ROS-related pathways were similar between groups, supporting ROS-independent MAPK/ERK activation. A caveat is that signaling and proliferation were measured in vitro in uSMC cultures derived from limited clinical samples. This paper is centrally about endometriosis and/or adenomyosis — it specifically demonstrates MAPK/ERK pathway activation in uterine smooth muscle cells of women with adenomyosis.
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- Transcriptome sequencing of adenomyosis eutopic endometrium: A new insight into its pathophysiology 2019
- Bioinformatics strategy for the screening of key genes to differentiate adenomyosis from endometriosis (Review) 2019
- Pathogenesis of adenomyosis: an update on molecular mechanisms 2017
- MicroRNA-17 downregulates expression of the PTEN gene to promote the occurrence and development of adenomyosis 2017
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