ArticleThe ocular surface2025
Corneal epithelial cells upregulate macropinocytosis to engulf metabolically active axonal mitochondria released by injured axons.
Article in The ocular surface, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons' Response toPathogens (Basel, Switzerland) · 2026Article
- The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons' Response tobioRxiv : the preprint server for biology · 2026Article
- Transmission Electron Microscopy Corneal Ultrastructure Study in Hematocornea of Corneal Transplant Graft.Diagnostics (Basel, Switzerland) · 2026Article
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Corneal Extracellular Vesicles: Small Packages with a Big Impact.Pharmaceutics · 2026Review
- Optimization and Application of Seahorse Glycolytic Stress Test in Mouse Corneal Tissues: Revealing Metabolic Profiles in Injury Models.Investigative ophthalmology & visual science · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
purposeTo determine the mechanisms used to internalize mitochondria by corneal epithelial cells after in vivo corneal trephine injury and in vitro in corneal epithelial cells.
methodsMale and female mice were subjected to trephine injury and euthanized immediately, 6, and 24 h after injury. Macropinocytosis was quantified in vivo using 70 kD fluorescent dextran. Mitochondrial content was assessed by immunofluorescence and metabolic activity quantified by Seahorse assay immediately and 6 h after injury. In vitro experiments using human corneal and limbal epithelial (HCLE) cells and isolated mitochondria were performed to assess mitochondrial transfer in the presence of the gap junction inhibitor 18α-glycyrrhetinc acid and the macropincytosis inhibitor ethylisopropylamiloride.
resultsMitochondria accumulate within apical epithelial cell layers within minutes of trephine injury. Macropinocytosis also increases within minutes of trephine injury. Oxygen Consumption Rates increase in the corneal epithelium 6 h after trephine injury in males and females. Inhibiting gap junctions increases mitochondrial engulfment while inhibiting macropinocytosis prevents engulfment of mitochondria by corneal epithelial cells in vitro.
conclusionsMolecules released by injured cells and severed axons induce macropinocytosis in corneal epithelial cells within minutes of trephine injury. An increase in oxygen consumption rate in the corneal epithelium after trephine injury indicates that axonal mitochondria can evade lysosomal degradation for at least 6 h. In vitro studies using isolated labeled and unlabeled mitochondria and control and mechanically stressed human corneal epithelial cells confirm the involvement of macropinocytosis in the engulfment of free and vesicle bound mitochondria by corneal epithelial cells.
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