AI Article Synopsis

  • Menstrual blood mesenchymal stem cells (MenSCs) are being studied for their potential in regenerative medicine, particularly in endometriosis, due to their noninvasive nature.
  • Research has shown that changes in miRNA regulation affect key cellular processes such as growth and differentiation in endometriotic MenSCs.
  • A study revealed that the expression of a crucial gene related to miRNA biosynthesis, DROSHA, is significantly reduced in endometriotic MenSCs, suggesting altered miRNA profiles that could influence disease progression.

Article Abstract

Menstrual blood mesenchymal stem cells (MenSCs) have gained prominence in the endometriosis scientific community, given their multifunctional roles in regenerative medicine as a noninvasive source for future clinical applications. In addition, changes in post-transcriptional regulation via miRNAs have been explored in endometriotic MenSCs with a role in modulating proliferation, angiogenesis, differentiation, stemness, self-renewal, and the mesenchymal-epithelial transition process. In this sense, homeostasis of the miRNA biosynthesis pathway is essential for several cellular processes and is related to the self-renewal and differentiation of progenitor cells. However, no studies have investigated the miRNA biogenesis pathway in endometriotic MenSCs. In this study, we profiled the expression of eight central genes for the miRNA biosynthesis pathway under experimental conditions involving a two-dimensional culture of MenSCs obtained from healthy women ( = 10) and women with endometriosis ( = 10) using RT-qPCR and reported a two-fold decrease in expression in the disease. In addition, miR-128-3p, miR-27a-3p, miR-27b-3p, miR-181a-5p, miR-181b-5p, miR-452-3p, miR-216a-5p, miR-216b-5p, and miR-93-5p, which have been associated with endometriosis, were identified through in silico analyses as negative regulators of . Because DROSHA is essential for miRNA maturation, our findings may justify the identification of different profiles of miRNAs with DROSHA-dependent biogenesis in endometriosis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10057010PMC
http://dx.doi.org/10.3390/ijms24065963DOI Listing

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