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Reprogramming the aging ovarian microenvironment via mitochondrial sharing and structural remodeling.

Chia-Jung Li1,2,3,4,5, Li-Te Lin1,2,4,6,7,8, Pei-Hsuan Lin1,4,6

  • 1Department of Obstetrics and Gynecology, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.

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Summary
This summary is machine-generated.

Cellular contact is vital for mitochondrial health in aging ovaries. Enhancing cell connections can restore mitochondrial function, offering a new strategy against reproductive aging.

Keywords:
Cell-cell communicationMitochondrial transferOvarian agingReproductive microenvironment

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Area of Science:

  • Reproductive Biology
  • Cellular Biology
  • Mitochondrial Biology

Background:

  • Mitochondrial dysfunction in ovarian granulosa cells (GCs) and cumulus cells (CCs) is a hallmark of reproductive aging, leading to decreased oocyte quality and fertility.
  • Impaired mitochondrial function in these cells contributes significantly to the decline in female reproductive capacity with age.

Purpose of the Study:

  • To investigate if enhancing cytoskeletal dynamics or cell-cell contact can restore mitochondrial function in aging ovarian cells.
  • To explore novel regenerative strategies for counteracting reproductive aging by improving mitochondrial health.

Main Methods:

  • Assessed mitochondrial exchange via tunneling nanotubes (TNTs) in human ovarian somatic cells using co-culture, live imaging, and mitochondrial labeling.
  • Modulated cytoskeletal dynamics with FTY720 and promoted cell-cell contact using 3D extracellular matrix (ECM) scaffolds.
  • Evaluated functional outcomes through ATP assays, mitochondrial membrane potential, Seahorse bioenergetics, transcriptomics, and in vivo studies in aged mice.

Main Results:

  • Mitochondrial transfer via TNTs between GCs and CCs diminishes with age; FTY720 treatment restored this transfer and improved cellular bioenergetics.
  • 3D ECM culture enhanced mitochondrial function and activated YAP signaling, demonstrating a non-pharmacological approach.
  • In aged mice, FTY720 treatment increased follicle count, improved oocyte mitochondrial quality, and raised anti-Müllerian hormone (AMH) levels.

Conclusions:

  • Somatic cell contact is crucial for mitochondrial complementation in aging ovaries, highlighting the importance of intercellular connectivity.
  • Reactivating endogenous mitochondrial sharing through cytoskeletal or microenvironmental modulation can restore bioenergetic function.
  • Targeting intercellular mitochondrial dynamics presents a promising regenerative strategy to combat reproductive aging and improve fertility outcomes.