Knockdown of DNMT1 Induces SLCO3A1 to Promote Follicular Growth by Enhancing the Proliferation of Granulosa Cells in Mammals

In female mammals, the proliferation and apoptosis of granulosa cells (GCs) have been shown to determine the fate of follicles. DNA methyltransferases (DNMTs) and have been reported to be involved in the survival of GCs and follicular growth. However, the molecular mechanisms enabling DNMTs to regul...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:International journal of molecular sciences 2024-02, Vol.25 (5), p.2468
Hauptverfasser: Li, Shuo, Zeng, Liqing, Miao, Fen, Li, Nian, Liao, Weili, Zhou, Xiaofeng, Chen, Yongcai, Quan, Hongyan, He, Yingting, Zhang, Hao, Li, Jiaqi, Yuan, Xiaolong
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:In female mammals, the proliferation and apoptosis of granulosa cells (GCs) have been shown to determine the fate of follicles. DNA methyltransferases (DNMTs) and have been reported to be involved in the survival of GCs and follicular growth. However, the molecular mechanisms enabling DNMTs to regulate the expression of to participate in follicular growth are unclear. In this study, we found that the knockdown of enhanced the mRNA and protein levels of by regulating the chromatin accessibility probably. Moreover, upregulated the mRNA and protein levels of , and to promote the proliferation of GCs and facilitated cell cycle progression by increasing the mRNA and protein levels of , and , but it decreased apoptosis by downregulating the mRNA and protein levels of and . Moreover, promoted the growth of porcine follicles and development of mice follicles. In conclusion, the knockdown of upregulated the mRNA and protein levels of , thereby promoting the proliferation of GCs to facilitate the growth and development of ovarian follicles, and these results provide new insights into investigations of female reproductive diseases.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms25052468