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Inhibition of miR-152 during In Vitro Maturation Enhances the Developmental Potential of Porcine Embryos. | LitMetric

AI Article Synopsis

  • The study investigates the role of the microRNA miR-152 in the developmental competence of porcine oocytes during maturation.
  • Inhibiting miR-152 improves the blastocyst formation rate, while overexpressing it leads to lower rates and alters the expression of quality-related genes.
  • The results suggest that miR-152 negatively impacts blastocyst rates possibly by targeting components of the IGF system, highlighting its importance in oocyte development.

Article Abstract

Oocyte developmental competence is regulated by various mechanisms and molecules including microRNAs (miRNAs). However, the functions of many of these miRNAs in oocyte and embryo development are still unclear. In this study, we managed to manipulate the expression level of miR-152 during oocyte maturation to figure out its potential role in determining the developmental competence of porcine oocytes. The inhibition (Inh) of miR-152 during oocyte maturation does not affect the MII and cleavage rates, however it significantly enhances the blastocyst rate compared to the overexpression (OvExp) and control groups. Pathway analysis identified several signaling pathways (including PI3K/AKT, TGFβ, Hippo, FoxO, and Wnt signaling) that are enriched in the predicted target genes of miR-152. Gene expression analysis revealed that was significantly up-regulated in the Inh group and downregulated in the OvExp group of oocytes. Moreover, was significantly upregulated in the Inh oocyte group compared to the control one and was downregulated in the Inh oocyte group compared to the other groups. Blastocysts developed from the OvExp oocytes exhibited an increase in miR-152 expression, dysregulation in some quality-related genes, and the lowest rate of blastocyst formation. In conclusion, our results demonstrate a negative correlation between miR-152 expression level and blastocyst rate in pigs. This correlation could be through targeting IGF system components during oocyte development.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7761803PMC
http://dx.doi.org/10.3390/ani10122289DOI Listing

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