Post-transcriptional silencing of Bos taurus prion family genes and its impact on granulosa cell steroidogenesis

Prion proteins constitute a major public health concern, which has partly overshadowed their physiological roles in several scenarios. Indeed, these proteins were implicated in male fertility but their role in female fertility is relatively less explored. This study was designed to evaluate the role of SPRN and PRNP prion family genes in bovine follicular steroidogenesis pathways. Post-transcriptional SPRN and PRNP silencing with siRNAs was established in bovine granulosa cell (GC) in vitro culture, and gene expression and progesterone and estradiol concentrations were evaluated. SPRN knockdown, led to a down regulation of CYP11A1 mRNA levels (2.1-fold), and PRNP knockdown led to an upregulation of SPRN mRNA levels (2.3-fold). CYP19A1 expression and estradiol synthesis was not detected in any experimental group. Finally, SPRN knockdown led to a mild reduction in progesterone production in GCs and this was the only experimental group that did not exhibit an increment in progesterone levels after 48 h of culture. As a conclusion, it was possible to detect the expression of the SPRN gene in bovine GCs, a potential interaction between SPRN and PRNP regulation, and the impact of SPRN expression on CYP11A1 and progesterone levels. These findings bring new insights into the role of these genes in ovarian steroidogenesis and female reproductive physiology. (c) 2022 Elsevier Inc. All rights reserved.

Automated summary

Prion proteins have been extensively studied in relation to male fertility, but their role in female fertility remains relatively unexplored. This study investigated the impact of SPRN and PRNP genes on bovine follicular steroidogenesis pathways. The findings suggest a potential interaction between SPRN and PRNP regulation, as well as the influence of SPRN expression on CYP11A1 and progesterone levels. These results provide new insights into the role of these genes in ovarian steroidogenesis and female reproductive physiology.