Endometriosis is a chronic systemic disease affecting ∼10–15% of women of reproductive age, often resulting in chronic pelvic pain and infertility. Despite its high prevalence, diagnosis is frequently delayed. tRNA-derived fragments (tRFs) are an emerging class of small non-coding RNAs that have been implicated in gene regulation and various pathological processes but remain understudied in endometriosis. This study aimed to characterize temporal changes in circulating tRF abundance after experimentally induced endometriosis in a baboon model. Endometriosis was induced in eight female baboons, and peripheral blood samples were collected at five time points post-inoculation. RNA was extracted from serum samples and sequenced to profile tRF abundance. Differential expression analysis was performed. Significant changes in tRFs were observed as early as 3 months after induction. A ranking based on log fold change and adjusted P-values revealed the 10 most significantly altered tRFs. These tRFs demonstrated consistent differential abundance throughout all time points. This is the first study to investigate circulating tRFs in endometriosis. Our longitudinal findings suggest that tRFs may serve as promising candidate biomarkers for endometriosis.

Induced abortions occur worldwide, accounting for approximately 53 million cases every year [1]. Medical abortion, defined as the intentional abortion through pharmacological methods, represents a ...

Endometriosis is a disease associated with pain symptoms and reduced fertility, characterized by the presence of endometrial tissue outside the uterus. SETD3 is an actin-specific histidine N-methyltransferase that regulates actin stability and flexibility. Here, we investigate the effects of altered SETD3 expression on cytoskeletal function and endometriotic cell motility. SETD3 expression in endometriotic lesions was analyzed using EndometDB, and in uteri of the superfertile Dummerstorf mouse line FL1 by RT-qPCR. The functional impact of siRNA-mediated SETD3 depletion on endometriotic 12Z cells and primary endometriotic stroma cells was studied in vitro. Cell motility, contractility, invasiveness, morphology and gene expression were analyzed by RT-qPCR, Western blotting, immunofluorescence, scratch wound, collagen contraction and Matrigel invasion assays. In patient tissue, SETD3 expression was slightly increased in deep endometriotic lesions, whereas SETD3 was downregulated 1.6-fold in the uteri of superfertile mice. SETD3 depletion delayed cell motility, reduced invasiveness of 12Z cells, and reduced the capability to contract collagen gels. Cytoskeletal gene expression was moderately changed. Our data suggest that the histidine N-methyltransferase SETD3 contributes to cytoskeletal remodeling that plays a key role in cell migration and invasion. A dysregulation of SETD3 could therefore be related to the pathogenesis of endometriosis, particularly in deep endometriosis.