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A single-cell atlas of the aging mouse ovary.

José V V IsolaSarah R OcañasChase R HubbartSunghwan KoSamim Ali MondalJessica D HenseHannah N C CarterAugusto SchneiderSusan KovatsJose Alberola-IlaWillard M FreemanMichael B Stout
Published in: Nature aging (2024)
Ovarian aging leads to diminished fertility, dysregulated endocrine signaling and increased chronic disease burden. These effects begin to emerge long before follicular exhaustion. Female humans experience a sharp decline in fertility around 35 years of age, which corresponds to declines in oocyte quality. Despite a growing body of work, the field lacks a comprehensive cellular map of the transcriptomic changes in the aging mouse ovary to identify early drivers of ovarian decline. To fill this gap we performed single-cell RNA sequencing on ovarian tissue from young (3-month-old) and reproductively aged (9-month-old) mice. Our analysis revealed a doubling of immune cells in the aged ovary, with lymphocyte proportions increasing the most, which was confirmed by flow cytometry. We also found an age-related downregulation of collagenase pathways in stromal fibroblasts, which corresponds to rises in ovarian fibrosis. Follicular cells displayed stress-response, immunogenic and fibrotic signaling pathway inductions with aging. This report provides critical insights into mechanisms responsible for ovarian aging phenotypes. The data can be explored interactively via a Shiny-based web application.
Keyphrases
  • single cell
  • rna seq
  • signaling pathway
  • flow cytometry
  • high throughput
  • induced apoptosis
  • oxidative stress
  • type diabetes
  • young adults
  • adipose tissue
  • peripheral blood