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Phosphoribosyl-pyrophosphate synthetase 2 (PRPS2) depletion regulates spermatogenic cell apoptosis and is correlated with hypospermatogenesis


1 Department of Urology, The First Affiliated Hospital of Jinan University, Guangzhou 510630, China
2 Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou 510060, China
3 Center for Reproductive Medicine, Guangdong Armed Police Hospital, Guangzhou Medical University, Guangzhou 510507, China
4 Department of Urology, Zhujiang Hospital of Southern Medical University, Guangzhou 510282, China

Correspondence Address:
Fang-Peng Shu,
Department of Urology, Zhujiang Hospital of Southern Medical University, Guangzhou 510282
China
Xiang-Ming Mao,
Department of Urology, Zhujiang Hospital of Southern Medical University, Guangzhou 510282
China
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aja.aja_122_19

PMID: 31736475

Phosphoribosyl-pyrophosphate synthetase 2 (PRPS2) is a rate-limiting enzyme and plays an important role in purine and pyrimidine nucleotide synthesis. Recent studies report that PRPS2 is involved in male infertility. However, the role of PRPS2 in hypospermatogenesis is unknown. In this study, the relationship of PRPS2 with hypospermatogenesis and spermatogenic cell apoptosis was investigated. The results showed that PRPS2 depletion increased the number of apoptotic spermatogenic cells in vitro. PRPS2 was downregulated in a mouse model of hypospermatogenesis. When PRPS2 expression was knocked down in mouse testes, hypospermatogenesis and accelerated apoptosis of spermatogenic cells were noted. E2F transcription factor 1 (E2F1) was confirmed as the target gene of PRPS2 and played a key role in cell apoptosis by regulating the P53/Bcl-xl/Bcl-2/Caspase 6/Caspase 9 apoptosis pathway. Therefore, these data indicate that PRPS2 depletion contributes to the apoptosis of spermatogenic cells and is associated with hypospermatogenesis, which may be helpful for the diagnosis of male infertility.


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