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We next examined whether these metabolic and viability phenotypes reflected defects in pre-mRNA splicing (Fig
UC-MSCs inhibit granulosa cell apoptosis through the activation of the AKT and P38 signaling pathways, while also down-regulating the expression of pro-inflammatory cytokines, such as IL-6 and IL-1, and up-regulating the expression of anti-inflammatory cytokines including IL-10, tumor necrosis factor- stimulated gene-6 (TSG-6), and VEGF
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