Moreover, reduced expression of PCNA was observed to significantly increase primordial follicle assembly, but these primordial follicles contained fewer guanulosa cells.
The second alternative possibility to increase primordial follicle reserve is a decrease in recruitment toward growth.
Thus, these data indicate that knockdown of PCNA in mouse ovaries around follicle formation increases primordial follicle assembly, but delays the transition of primordial to primary follicles.
Inhibition of the increased expression of PCNA in ovaries around primordial follicle formation alleviates apoptosis of oocytes and increases primordial follicle assembly.
Our approach was based on recent studies showing that two different histone deacetylase inhibitors, trichostatin-A and suberoylanilide hydroxamic acid, increase primordial follicle numbers in adult female mice through denovo oogenesis [ 15, 16].
Recently, the distinct expression of PCNA was reported with the development of fetal and newborn rat ovaries, with PCNA-positive oocytes observed at high percentages from 14.5 dpc to 1 day post-partum (dpp), decreasing after birth, and increasing during primordial follicle formation [22].
The rise in AMH and inhibin B levels during prepubertal childhood supports the intriguing concept that increasing ovarian primordial follicle recruitment and follicle activity precedes the onset of central puberty.
