Overexpression of Pde4d in rat granulosa cells inhibits maturation and atresia of antral follicles to induce polycystic ovary

Lu‐Yang Jin, Lu-Yang Jin, Jiaen Yu, Jia-En Yu, Hai-Yan Xu, Haiyan Xu, Bin Chen, Qian Yang, Ye Liu, Meng-Xi Guo, Mengxi Guo, Cheng-Liang Zhou, Chengliang Zhou, Yi Cheng, Haiyan Pang, Hai-Yan Pang, Haiyan Wu, Hai-Yan Wu, Jian‐Zhong Sheng, Jian-Zhong Sheng, Hefeng Huang, He-Feng Huang
Biochimica et biophysica acta. Molecular basis of disease · 2023 · vol. 1870(1) , pp. 166869 · doi:10.1016/j.bbadis.2023.166869 · PMID:37673361 · W4386419498
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Overexpression of Pde4d in rat granulosa cells inhibits antral follicle maturation and atresia, thereby inducing a polycystic ovary phenotype.

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Abstract

BACKGROUND: Follicle dysplasia can cause polycystic ovary syndrome, which can lead to anovulatory infertility. This study explored gene(s) that may contribute to polycystic ovary syndrome. METHODS: Three animal models of polycystic ovary syndrome were created by treating 3-week-old rats respectively with estradiol valerate, testosterone propionate, or constant illumination for 8 weeks. Granulosa cells from the three disease groups and from healthy controls were transcriptionally profiled to identify differentially expressed genes. The phosphodiesterase-4d (Pde4d) was screened as the most promising candidate pathogenic gene. The Pde4d was overexpressed in rats via intrabursal infection with recombinant lentivirus to see the effect of Pde4d on ovarian morphology. The potential roles of the candidate gene and interactors of the encoded protein were explored using polymerase chain reaction, western blotting, transfection and co-immunoprecipitation. RESULTS: All three rat models of polycystic ovary syndrome showed polycystic ovary phenotype. Seven promising candidate genes were obtained by transcriptomics and verifications. Pde4d was further investigated because it could trigger downstream signaling pathways. The Pde4d overexpression in rat ovary induced cystic follicles. It inhibited follicle maturation through a mechanism involving inhibition of cAMP-PKA-CREB signaling. The Pde4d also inhibited phosphorylation of c-Jun N-terminal kinase to reduce apoptosis in the ovary, through a mechanism involving interaction of its poly-proline domain with the protein POSH. CONCLUSION: Upregulation of Pde4d may contribute to polycystic ovary syndrome by impeding follicle maturation and preventing apoptotic atresia.

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MeSH descriptors

Polycystic Ovary Syndrome Polycystic Ovary Syndrome Polycystic Ovary Syndrome Animals Cyclic Nucleotide Phosphodiesterases, Type 4 Female Granulosa Cells Granulosa Cells Ovarian Follicle Ovarian Follicle Ovarian Follicle Phosphoric Diester Hydrolases Phosphoric Diester Hydrolases Rats

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