Genomic profiling of spermatogonial stem cells and embryonic stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE38776 | GEO | 2021/05/23
REPOSITORIES: GEO
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Project description:Because spermatogonial stem cells (SSCs) are virtually immortal by serial transplantation, SSC decrease in aged testes is considered to be caused by deteriorated microenvironment. Here we report cell-intrinsic mode of SSC aging. SSCs cultured for 5 years proliferate more actively than young SSCs and showed enhanced glycolytic activity but remain euploid and exhibited stable androgenetic imprinting patterns. Moreover, the aged SSCs kept constant SSC activity despite shortened telomeres. The increased proliferative activity of aged SSCs was caused by Wnt7b expression, which likely occurred due to decreased polycomb complex2 activity. Aberrant Wnt7b expression not only decreased reactive oxygen species levels and mitochondria activity but also stimulated glycolysis via c-jun N-terminal kinase (JNK) activation. Analysis of SSCs in Klotho aging mouse model also confirmed hyperactivation of JNK pathway and increased glycolysis. Therefore, not only SSC microenvironment but also intrinsic activation of Wnt7b-mediated glycolysis plays important roles in SSC aging.
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Project description:The spermatogonial stem cells (SSCs) niche is critical for SSC maintenance and the subsequent spermatogenesis. Numerous reproductive hazards impair the SSC niche, thereby result in aberrant SSC self-renewal and male infertility. However, promising agents targeting the impaired SSC niche to promote SSC self-renewal are still limited. Here, we screen out and assess the effects of Lovastatin on the self-renewal of mouse spermatogonial stem cells (mSSCs). Mechanistically, Lovastatin promotes the self-renewal of mSSCs and inhibits its inflammation and apoptosis through the regulation of isoprenoid intermediates. Likewise, other statins exhibit similar effects on SSC self-renewal. Remarkably, the treatment by Lovastatin could promote the self-renewal of mSSCs in the male gonadotoxicity model generated by busulfan injection. Noteworthy, we demonstrate that Lovastatin could significantly enhance the self-renewal of in vitro cultured primate SSCs. Collectively, our findings uncover that lovastatin could promote the self-renewal of both murine and primate SSCs and have implications for the treatment of certain male infertility using small compounds.
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