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Autori principali: Li, Chia-Jung, Lin, Li-Te, Lin, Pei-Hsuan, Sheu, Jim Jinn-Chyuan, Wen, Zhi-Hong, Tsui, Kuan-Hao
Natura: Artículo científico
Lingua:en
Pubblicazione: Theranostics 2025
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Accesso online:https://pubmed.ncbi.nlm.nih.gov/40963898/
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author Li, Chia-Jung
Lin, Li-Te
Lin, Pei-Hsuan
Sheu, Jim Jinn-Chyuan
Wen, Zhi-Hong
Tsui, Kuan-Hao
author_facet Li, Chia-Jung
Lin, Li-Te
Lin, Pei-Hsuan
Sheu, Jim Jinn-Chyuan
Wen, Zhi-Hong
Tsui, Kuan-Hao
Li, Chia-Jung
Lin, Li-Te
Lin, Pei-Hsuan
Sheu, Jim Jinn-Chyuan
Wen, Zhi-Hong
Tsui, Kuan-Hao
collection PubMed - marine biology
contents Reprogramming the aging ovarian microenvironment via mitochondrial sharing and structural remodeling. Li, Chia-Jung Lin, Li-Te Lin, Pei-Hsuan Sheu, Jim Jinn-Chyuan Wen, Zhi-Hong Tsui, Kuan-Hao Female Animals Mitochondria Mice Humans Aging Granulosa Cells Ovary Cumulus Cells Oocytes Fingolimod Hydrochloride Membrane Potential, Mitochondrial Extracellular Matrix Cytoskeleton Cellular Microenvironment Coculture Techniques Cell Communication Mitochondrial dysfunction in ovarian granulosa cells (GCs) and cumulus cells (CCs) is a defining feature of reproductive aging, contributing to impaired oocyte quality and reduced fertility. This study investigates whether enhancing cytoskeletal dynamics or promoting structural contact between cells can restore mitochondrial function and mitigate ovarian aging. Mitochondrial exchange was assessed using co-culture systems, live-cell imaging, and mitochondrial labeling in human ovarian somatic cells. Cytoskeletal modulation was achieved using FTY720, and cell-cell contact was enhanced through soft 3D extracellular matrix (ECM) scaffolds. Functional outcomes were evaluated through ATP assays, mitochondrial membrane potential, Seahorse bioenergetics profiling, and transcriptomic analysis. In vivo validation was conducted in aged mice treated with FTY720. Granulosa and cumulus cells exchanged mitochondria via tunneling nanotubes (TNTs), a process significantly reduced with age. Mitochondrial transfer was contact-dependent and not mediated by paracrine signaling. FTY720 enhanced TNT formation and mitochondrial delivery, restoring ATP levels, membrane potential, and oxidative phosphorylation in aged cells. 3D ECM culture promoted spheroid formation, activated YAP signaling, and improved mitochondrial function without pharmacological agents. In aged mice, FTY720 treatment increased follicle numbers, improved oocyte mitochondrial quality, and elevated serum AMH levels. These findings demonstrate that somatic cell contact is essential for mitochondrial complementation in aging ovaries. By promoting intercellular connectivity through cytoskeletal or microenvironmental remodeling, endogenous mitochondrial sharing can be reactivated to restore bioenergetic function. This approach offers a novel regenerative strategy to counteract reproductive aging.
format Artículo científico
id pubmed_40963898
institution PubMed
language en
publishDate 2025
publisher Theranostics
record_format pubmed
spellingShingle Reprogramming the aging ovarian microenvironment via mitochondrial sharing and structural remodeling.
Li, Chia-Jung
Lin, Li-Te
Lin, Pei-Hsuan
Sheu, Jim Jinn-Chyuan
Wen, Zhi-Hong
Tsui, Kuan-Hao
Female
Animals
Mitochondria
Mice
Humans
Aging
Granulosa Cells
Ovary
Cumulus Cells
Oocytes
Fingolimod Hydrochloride
Membrane Potential, Mitochondrial
Extracellular Matrix
Cytoskeleton
Cellular Microenvironment
Coculture Techniques
Cell Communication
Reprogramming the aging ovarian microenvironment via mitochondrial sharing and structural remodeling. Li, Chia-Jung Lin, Li-Te Lin, Pei-Hsuan Sheu, Jim Jinn-Chyuan Wen, Zhi-Hong Tsui, Kuan-Hao Female Animals Mitochondria Mice Humans Aging Granulosa Cells Ovary Cumulus Cells Oocytes Fingolimod Hydrochloride Membrane Potential, Mitochondrial Extracellular Matrix Cytoskeleton Cellular Microenvironment Coculture Techniques Cell Communication Mitochondrial dysfunction in ovarian granulosa cells (GCs) and cumulus cells (CCs) is a defining feature of reproductive aging, contributing to impaired oocyte quality and reduced fertility. This study investigates whether enhancing cytoskeletal dynamics or promoting structural contact between cells can restore mitochondrial function and mitigate ovarian aging. Mitochondrial exchange was assessed using co-culture systems, live-cell imaging, and mitochondrial labeling in human ovarian somatic cells. Cytoskeletal modulation was achieved using FTY720, and cell-cell contact was enhanced through soft 3D extracellular matrix (ECM) scaffolds. Functional outcomes were evaluated through ATP assays, mitochondrial membrane potential, Seahorse bioenergetics profiling, and transcriptomic analysis. In vivo validation was conducted in aged mice treated with FTY720. Granulosa and cumulus cells exchanged mitochondria via tunneling nanotubes (TNTs), a process significantly reduced with age. Mitochondrial transfer was contact-dependent and not mediated by paracrine signaling. FTY720 enhanced TNT formation and mitochondrial delivery, restoring ATP levels, membrane potential, and oxidative phosphorylation in aged cells. 3D ECM culture promoted spheroid formation, activated YAP signaling, and improved mitochondrial function without pharmacological agents. In aged mice, FTY720 treatment increased follicle numbers, improved oocyte mitochondrial quality, and elevated serum AMH levels. These findings demonstrate that somatic cell contact is essential for mitochondrial complementation in aging ovaries. By promoting intercellular connectivity through cytoskeletal or microenvironmental remodeling, endogenous mitochondrial sharing can be reactivated to restore bioenergetic function. This approach offers a novel regenerative strategy to counteract reproductive aging.
title Reprogramming the aging ovarian microenvironment via mitochondrial sharing and structural remodeling.
topic Female
Animals
Mitochondria
Mice
Humans
Aging
Granulosa Cells
Ovary
Cumulus Cells
Oocytes
Fingolimod Hydrochloride
Membrane Potential, Mitochondrial
Extracellular Matrix
Cytoskeleton
Cellular Microenvironment
Coculture Techniques
Cell Communication
url https://pubmed.ncbi.nlm.nih.gov/40963898/