Research Paper Volume 13, Issue 7 pp 9348—9372
miR-30c-1 encourages human corneal endothelial cells to regenerate through ameliorating senescence
- 1 Department of Ophthalmology, Hallym University Medical Center, Hallym University College of Medicine, Seoul, Republic of Korea
Received: May 11, 2020 Accepted: February 16, 2021 Published: March 19, 2021https://doi.org/10.18632/aging.202719
How to Cite
Copyright: © 2021 Bae et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In the present study, we studied the role of microRNA-30c-1 (miR-30c-1) on transforming growth factor beta1 (TGF-β1)-induced senescence of hCECs. hCECs were transfected by miR-30c-1 and treated with TGF-β1 to assess the inhibitory effect of miR-30c-1 on TGF-β1-induced senescence. Cell viability and proliferation rate in miR-30c-1-transfected cells was elevated compared with control. Cell cycle analysis revealed that cell abundance in S phase was elevated in miR-30c-1-treated cells compared with control. TGF-β1 increased the senescence of hCECs; however, this was ameliorated by miR-30c-1. TGF-β1 increased the size of hCECs, the ratio of senescence-associated beta-galactosidase-stained cells, secretion of senescence-associated secretory phenotype factors, the oxidative stress, and arrested the cell cycle, all of which were ameliorated by miR-30c-1 treatment. miR-30c-1 also suppressed a TGF-β1-induced depolarization of mitochondrial membrane potential and a TGF-β1 stimulated increase in levels of cleaved poly (ADP-ribose) polymerase (PARP), cleaved caspase 3, and microtubule-associated proteins 1A/1B light chain 3B II. In conclusion, miR-30c-1 promoted the proliferation of hCECs through ameliorating the TGF- β1-induced senescence of hCECs and reducing cell death of hCECs. Thus, miR-30c-1 may be a therapeutic target for hCECs regeneration.