Abstract
Aims/Purpose: The study aims to elucidate the potential role of TNT‐mediated intercellular communication between the AdMSCs and RPE‐1 cells in reducing stress‐induced damage.Methods: Oxidative stress and serum starvation were used as stress to create TNTs between the AdMSC and RPE‐1 cells. Immunofluorescence and scanning electron microscopy were used to show that TNT formation. Following stress conditions, the cells' viability was examined by CTG assay, and the levels of reactive oxygen species (ROS) were measured by H2DCFH‐DA probes. Microscopy showed that JC‐1 labelled mitochondrial exchange occurs between cells via TNTs. To prevent TNTs, a transmembrane culture system was used and evaluated how to effect on cell viability and changes of ROS levels.Results: We examined how TNTs support mitochondrial transport and intercellular communication between AdMSCs and RPE‐1 during stress. We discovered that TNT‐mediated mitochondrial translocation from AdMSCs to RPE‐1 contributes to both increased cell survival and a decrease in ROS levels. We showed that AdMSCs and RPE‐1 had a direct connection that was essential for stress recovery. After stress‐induced damage, co‐culture improved vitality and maintained retinal function. Because mechanical restriction of TNT synthesis reduced cell viability and raised ROS levels, it is clear that TNTs are essential for cellular defence.Conclusions: Overall, our study provides valuable insights into the cellular mechanisms underlying stress response and underscores the therapeutic promise of AdMSC derived TNTs in preserving retinal health.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call