A single-cell atlas of the aging mouse ovary.
Autor: | Isola JVV; Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA., Ocañas SR; Genes & Human Disease Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.; Neuroscience Department, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.; Physiology Department, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.; Oklahoma City Veterans Affairs Medical Center, Oklahoma City, OK, USA., Hubbart CR; Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA., Ko S; Genes & Human Disease Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.; Neuroscience Department, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA., Mondal SA; Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA., Hense JD; Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.; Nutrition College, Federal University of Pelotas, Pelotas, Brazil., Carter HNC; Arthritis & Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA., Schneider A; Nutrition College, Federal University of Pelotas, Pelotas, Brazil., Kovats S; Arthritis & Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA., Alberola-Ila J; Arthritis & Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA., Freeman WM; Genes & Human Disease Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.; Oklahoma City Veterans Affairs Medical Center, Oklahoma City, OK, USA., Stout MB; Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. michael-stout@omrf.org.; Oklahoma City Veterans Affairs Medical Center, Oklahoma City, OK, USA. michael-stout@omrf.org. |
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Jazyk: | angličtina |
Zdroj: | Nature aging [Nat Aging] 2024 Jan; Vol. 4 (1), pp. 145-162. Date of Electronic Publication: 2024 Jan 10. |
DOI: | 10.1038/s43587-023-00552-5 |
Abstrakt: | 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. (© 2024. The Author(s).) |
Databáze: | MEDLINE |
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