Research Paper Volume 12, Issue 12 pp 12324—12341

Ovarian aging increases small extracellular vesicle CD81+ release in human follicular fluid and influences miRNA profiles

Figure 7. Hypothetical model of miRNAs mediating the regulation of TP53 in the ovarian follicle in female reproductive aging. Potential mechanisms by which specific ovarian follicle cell subpopulations can send and receive stress signaling, via EVs, in ovarian aging. MiR-155 expression is induced by stress in granulosa cells. TP53 activation, mediated by the downregulation of miR-16 and miR-214, can initiate apoptosis or lead to cellular senescence and the activation of miR-372 or cause the increase of EV secretion. The upregulation of miR-125 and the downregulation of miR-449 could represent a defense mechanism implemented by follicular cells and oocyte to repress TP53 expression and stress-induced apoptosis.