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A p-Tyr42 RhoA Inhibitor Promotes the Regeneration of Human Corneal Endothelial Cells by Ameliorating Cellular Senescence. | LitMetric

AI Article Synopsis

  • * Researchers investigated the effects of a p-Tyr42 RhoA inhibitor (MH4) on hCECs subjected to senescence-inducing conditions from TGF-β or HO, observing improvements in cell shape, proliferation, and adhesion.
  • * Findings suggest that MH4 enhances hCEC regeneration by counteracting the senescence effects of TGF-β and HO, specifically through the ROS/NF-κB/mitochondrial pathway, thus promoting healthier cell function.

Article Abstract

The development of treatment strategies for human corneal endothelial cells (hCECs) disease is necessary because hCECs do not regenerate in vivo due to the properties that are similar to senescence. This study is performed to investigate the role of a p-Tyr42 RhoA inhibitor (MH4, ELMED Inc., Chuncheon) in transforming growth factor-beta (TGF-β)- or HO-induced cellular senescence of hCECs. Cultured hCECs were treated with MH4. The cell shape, proliferation rate, and cell cycle phases were analyzed. Moreover, cell adhesion assays and immunofluorescence staining for F-actin, Ki-67, and E-cadherin were performed. Additionally, the cells were treated with TGF-β or HO to induce senescence, and mitochondrial oxidative reactive oxygen species (ROS) levels, mitochondrial membrane potential, and NF-κB translocation were evaluated. LC3II/LC3I levels were determined using Western blotting to analyze autophagy. MH4 promotes hCEC proliferation, shifts the cell cycle, attenuates actin distribution, and increases E-cadherin expression. TGF-β and HO induce senescence by increasing mitochondrial ROS levels and NF-κB translocation into the nucleus; however, this effect is attenuated by MH4. Moreover, TGF-β and HO decrease the mitochondrial membrane potential and induce autophagy, while MH4 reverses these effects. In conclusion, MH4, a p-Tyr42 RhoA inhibitor, promotes the regeneration of hCECs and protects hCECs against TGF-β- and HO-induced senescence via the ROS/NF-κB/mitochondrial pathway.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10295357PMC
http://dx.doi.org/10.3390/antiox12061186DOI Listing

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